Make your own free website on Tripod.com
ALNICOLSA del Perú S.A.C.

VENTANILLA - CALLAO (PERÚ)
Telefax.511. 553.0981.  E-mail. lebr7@yahoo.com

lebr7@yahoo.com

Página principal
• 
Indice de productos
• Venta de productos
• 
Páginas peruanas
• Venta de Maquinarias
• 
Revistas en texto completo
• Más Monografias
• 
ENLACES

Bienvenid@s a La Página Virtual de ALNICOLSA del Perú S.A.C.  Telf: 5530981 - Ultima Actualización

EL AJI

LA ESPECIA DEL NUEVO MUNDO

PROPIEDADES DE LA HORTALIZA PERUANA

INTRODUCCION 

El picante título no deja terreno sin explorar. Los origenes, el paso a través de la historia, las propiedades condimenticias, medicinales y socializantes, las múltiples especies, la composición química, el mecanismo del dolor, así como las actitudes culturales y sociales que se dan en el Perú y el mundo alrededor de esta planta.

El género Capsicum, que incluye entre 20 a 30 especies, tiene su centro de origen en las regiones tropicales y subtropicales de América, probablemente en el área Bolivia-Perú, donde se han encontrado semillas de formas ancestrales de más de 7.000 años, y desde donde se habría diseminado a toda América. Al menos cinco de sus especies son cultivadas en mayor o menor grado pero, a nivel mundial al igual que en Perú, casi la totalidad de la producción de ají y pimiento está dada por una sola especie, Capsicum annuum. Esto tiende a confundir porque a partir de esta especie se generan dos productos distintos para el consumidor: ají (del arawak axi) o fruto picante, y pimiento (de pimienta, por equivocación de C. Colón) o frutos no picantes. Los términos españoles pimentón y paprika deben reservarse para el producto seco y molido de la especie.

Es necesario destacar que existen otras especies del género cuyo fruto o producto también es denominado ají, y solo tienden a hacer más confusa la situación. Estas especies de interés más puntual son Capsicum chinense, cuyo cultivar "Habanero" produce el ají más picante que se conoce, Capsicum frutescens, cuyo cultivar "Tabasco" es muy usado para la elaboración de salsa picante y pickles, Capsicum baccatum, cuyo producto es conocido como ají andino y es ampliamente cultivado en las zonas altiplánicas, y Capsicum pubescens, cuyo cultivar "Rocoto" (Manzano y Siete Caldos son sinónimos) es muy apreciado por su sabor y picantez en diversas regiones de América.

Habanero

Tabasco

Aji amarillo

Capsicum chinense Capsicum frutescens Capsicum baccatum

Rocoto

Capsicum pubescens

Después del descubrimiento de América todas estas especies, principalmente Capsicum annuum, han sido llevadas a distintas regiones del mundo y rápidamente han pasado a ser la principal "especia" o condimento de comidas típicas de muchos países, por lo que su cultivo, aunque generalmente reducido en superficie, se encuentra ampliamente extendido, siendo Perú, China, Estados Unidos y México los principales productores a nivel mundial.

"El enamoramiento de los peruanos con el ají es largo e ininterrumpido" dice Cabieses. Cerámicas y textiles prehispánicos retratan al ardiente condimento como una planta de gran importancia no sólo como alimento sino en contextos mágicos y religiosos.

Ucho, el nombre de uno los Hermanos Ayar, la dinastía fundadora del imperio incaico, significa ají. Unido a Cachi: sal; Auca: guerrero; y Manco el jefe fundador, conforman los factores que fueron esenciales para la fundación del gran imperio

Sal y ají eran entonces los acompañantes obligatorios de todo alimento, como lo siguen siendo hoy. El ají es el condimento más generalizado en el mundo entero. Su presentación natural varía en tamaño, forma, color y calidad. Se usa fresco o procesado en diversas formas, seco, ahumado, entero, picado o molido; congelado, enlatado o envasado; con vinagre o sin él, en salmuera o en una variedad impresionante de salsas y preparados.

Aunque en otros países existan diferentes vocablos para referirse a las distintas variedades en el Perú se utiliza la palabra ají para referirse a todo fruto clasificado dentro del género  capsicum.

Ají amarillo

Todas las especies de ají son originaria de America y en la colonia los ajís fueron llevados a españa, desde donde se dispersaron a toda Europa y de allí al resto del mundo. Es más, algunas variedades de ají que llegaron a Estados Unidos fueron introducida por los inmigrantes europeos, en ves de haber llegado directamente de sudamérica o México.

En el Perú, el cultivo del ají esta muy difundido dado que el área de cultivo que ocupa nos representa del 6 al 7% del área total cultivada de hortalizas (Vallejo,1974).
En el ámbito mundial se destinan 986,00 ha. para su cultivo, totalizando una producción de 7'205,000 TM con un rendimiento promedio de 7,308 Kg./Ha.. En el Perú se cultivan más de 2,000 Ha. con una producción promedio de 5,532 Kg./Ha.. Las zonas donde se producen en mayor escala son los valles de Lima, Chincha, Cañete, Tacna, Oxapampa y Cerro de Pasco (Ortiz, 1983)
En el país se cultivan diferentes variedades de ají, en las tres regiones, donde existen muchas áreas agrícolas aptas para la producción comercial se realiza como cultivo anual debido a la fuerte incidencia de hongos que maltratan a las plantas (Capsicum pubescens), existiendo también en la Sierra, pero en menor escala (Corrales,1980)
Actualmente por sus propiedades pungentes (picante) y aromáticas se le utiliza seco, base para las salsas y pastas, estimulante digestivo, sazonador, como antioxidante en carnes y otros; lo que demuestra ser un recurso de amplísimo rango de aprovechamiento para su industrialización y menor pérdida con relación al fruto fresco.
El Concejo Internacional de Recursos Fitogenéticos con sede en Costa Rica, desde 1979 ha reconocido a nivel mundial la importancia socio económica y científica del género Capsicum, al cual pertenece el rocoto, siendo considerado dentro de los recursos fitogenéticos de primera prioridad, recomendando su recolección, evaluación en la estabilización y conservación (Ortiz,1983)

DESCRIPCION DEL ROCOTO

El cultivo del rocoto se remonta desde épocas pre-incas hasta la actualidad, es el principal condimento de nuestras comidas, usado principalmente por su sabor pungente (picante) sin que muchas veces se tenga idea del valor alimenticio, específicamente vitamínico y el papel importante que por ello podría estar desempeñando en la dieta diaria nacional, aún cuando sea usado en pequeñas proporciones (Vallejo 1968).
El nombre científico Capsicum pubescens, su nombre comercial es rocoto perteneciendo a la familia Solanáceas, generalmente las zonas de producción son los valles andinos, la época de siembra es todo el año teniendo como ámbito un clima templado, favoreciendo una temperatura óptima que fluctúa entre los 18 a 20° C con una humedad relativa baja.

La cosecha se realizará cuando presente una coloración de fruto verde o maduro. Con buena manipulación agrícola se llega a rendimientos de 200,000 frutos/Ha. (Orbegoso,1954).

En cuanto a la duración del poder germinativo de la semilla de ají es necesario utilizar semilla de un año o máximo de tres, conservada 7 días en lugares frescos y ventilados por 20 días a una temperatura de 10° C y humedad de 80% (Corrales, 1980).
El fruto es una baya seca aunque son frecuentes las variedades provistas de pulpa algo jugosas; en cuanto a forma, tamaño y color de los frutos, es muy variable según sus características genéticas; el tamaño en cuanto a la variedad es inconstante, al iniciarse la cosecha pueden ser de tamaño notablemente mayor que al término de ésta(Velasco,1971).

ORIGEN DE LA HORTALIZA

Lippert,(1926) señala que el origen del género Capsicum corresponde al nuevo mundo, teniéndose referencias de bayas secas encontradas en tumbas del Perú con antigüedad de 2,000 años.
Vavilov señala que el género Capsicum es de origen centro americano, correspondiendo su ubicación al Centro de Origen VII (México y Centro América) . El Perú por albergar gran variedad de especies tanto silvestres como cultivadas, es considerado como Centro de Origen Secundario ya que cuenta con todos los recursos apropiados para su fertilidad y expectativas de abundante producción.
Orbegoso,(1954) menciona que el género Capsicum puede derivarse de la palabra CAPSA (Caja) teniendo como referencia la forma del fruto; mientras que Velasco(1971) señala que el nombre proviene de la palabra CAPTO (morder) por su naturaleza picante.
León, (1968) describe a las plantas del género Capsicum como herbácea o arbustiva, de tronco leñoso y ramificación dicatómica, con hojas alternadas, lisas y brillantes, excepto en C. pubesces, que presenta hojas rugosas pubescentes.

CLASIFICACION SISTEMATICA QUE REPORTA ALVISTUR(1975)

División : Fanerógamas o Spermofitas (Strasburger 1963) o Antofitas (Coronado 1960)
Sub división : Angiospermas
Clase : Dicotiledoneas
Sub clase : Simpétalas o gamopétalas(Bayluy,1928)
Orden : Tumifloras
Sub Orden : Solanineas
Familia : Solanáceas
Tribu : Solanineas
Género : Capsicum
Especie : Capsicum pubescens R y P
Nombre Común : Rocoto

COMPOSICION DE LA HORTALIZA

Análisis dietéticos practicados por el Departamento de Nutrición del Ministerio de Salud del Perú(1978) le asignan los siguientes valores:
Por 100 gr., de peso neto Mínimo  Máximo
Agua 20.7 gr. 93.1 gr.
Hidratos de Carbono  5.3 gr 63.8 gr.
Proteínas 0.8 gr 6.7 gr.
Extracto etéreo  0.3 gr. 0.8 gr.
Fibra. 1.4 gr. 23.2 gr.
Cenizas  0.6 gr 7.1 gr.
Calcio 7.0 mg 116.0 mg

Fósforo

31.0 mg 200.0 mg
Hierro 1.3 mg 15.1 mg
Caroteno 0.03 mg. 25.2 mg
Tiamina 0.03 mg. 1.09 mg
 Riboflabina  0.07 mg 1.73 mg
Niacina 0.75 mg. 3.30 mg
Ac. ascórbico 14.4 mg 157.5 mg
Calorías 23 233
Capcisina 150 mg 335 mg por 10 gr./peso

 ESPECIES CULTIVADAS EN EL PERU

Las especies del género Capsicum, que incluye todas las variedades de ají, tanto dulces (pimiento) como picantes (rocoto), han sufrido diversas modificaciones en su clasificación siendo la más reciente, la aprobada en la Reunión de Consulta sobre recursos fitogenéticos de Capsicum, en Costa Rica el año 1980. En ella se determinó que son cinco las especies cultivadas :

 NOMBRE CIENTIFICO ..................... NOMBRE COMUN  Y PROCEDENCIA 

C. annuum (Mex y EEUU) .................. Dulce (pimiento)...picante(Chile)
C. chinense(Arequipa, La Molina) ........ Ají panca, limo 
C. frutescens (Piura) .......................... Ají arnaucho, mono
C. baccatum (La Libertad) .................. Ají escabeche o mirasol
C. pubescens (Lima)............................Rocoto 

BIBLIOGRAFIA:

-,Ch.C.(1962) "Composición de los Alimentos Peruanos" Instituto de Nutrición tercera edición Lima-Perú.
-Chiappe,L (1960) "Estudio comparativo de diversas variedades de ají" Tesis de Grado. LM.
-Corrales,N.(1961) "El cultivo del Ají en el Perú" Estación Experimental de Agricultura. La Molina.
-Delgado,D.F (1988) "Cultivos Hortícolas datos básicos" Edi-Agraria Universidad.
-ITINTEC norma técnica :
209.238-1986 "Salsa de Ají"
209.035-1970 "Pimentón"
209.070-1970 "Vinagre"
209.132-1986 "Determinación de Ceniza"
209.102-1975 "Especies y Condimentos"
203.071-1975 "Productos elaborados a partir de frutas y otros vegetales.

-Orbegoso,A(1954) "Reseña del Cultivo, identificación botánica y comparativo de rendimiento en fresco de variedades de ají Escuela Nacional de Agricultura. La Molina.
-Ortiz,R(1983) Utilización de descriptores en la caracterización de líneas de Capsicum.UNA
-Velasco,F.(1971) "Recolección y descripción de muestras del G. Capsicum en la provincia de Satipo (Junin) y San Miguel (Cajamarca).UNA.


 

Chemical characterisation

Name: Capsaicin (N-(4-hydroxy-3-methoxybenzyl)-8-methyl-trans-6-nonenamide)

Synonyms: 8-Methylnon-6-enoyl-4-hydroxy-3-methoxybenzylamide; trans-8- methyl-N-vanillyl-6-nonenamide; Isodecenoic acid vanillylamide

FL No:        16.014

CAS No:     404-86-4

FEMA No: 3404

CoE No:     2299

EINECS:     206-969-8

Structure:

Capsaicin in Capsicum preparations is always accompanied by other capsaicinoids: mainly dihydrocapsaicin, but also small amounts of nordihydro-, homo-, homodihydro-, nor-, and nornorcapsaicin. The capsaicinoids present in the Capsicum fruit are predominantly capsaicin and dihydrocapsaicin, making up 80 to 90%. The ratio of capsaicin to dihydrocapsaicin is generally around 1:1 and 2:1 (Govindarajan and Sathyanarayana, 1991).

Exposure assessment

Capsaicinoids are mainly ingested as naturally occurring pungency-producing components of capsicum spices (chilli, cayenne pepper, red pepper). They typically range from 0.1 mg/g in chilli pepper to 2.5 mg/g in red pepper and 60 mg/g in oleoresin red pepper (Parrish, 1996).

Pepper varieties from Capsicum frutescens, annuum and chinense were found to contain 0.22 - 20 mg total capsaicinoids/g of dry weight (Thomas et al., 1998). Cayenne pepper samples had mean capsaicin and dihydrocapsaicin contents of 1.32 and 0.83 mg/g dry weight, respectively (Lopez-Hernandez, 1996).

The consumption of capsicum spices was reported to be 2.5 g/person/day in India, 5 g/person/day in Thailand (Monsereenusorn, 1983) and 20 g/person (one chilli pepper) per day in Mexico (Lopez-Carrillo, 1994). Assuming a content of capsaicinoids in these spices of about 1%, the daily intake of capsaicinoids in these countries has been estimated to be 25 - 200 mg/person/day or in the case of a person with 50 kg body weight 0.5 – 4 mg/kg bw/day (Council of Europe, 2001).

The maximum daily intake of capsaicin in the U.S. and Europe from mild chillies and paprika was roughly estimated to be 0.025 mg/kg bw (Govindarajan and Sathyanarayana, 1991), equivalent to 1.5 mg/person/day. According to a recent estimation, the mean and maximum intake of capsaicin from industrially prepared food products containing the recommended general limit of 5 ppm would be 0.77 and 2.64 mg/day, respectively (CREDOC/OCA, 1998).

Hazard identification/characterisation

Capsaicin and other members of the group of capsaicinoids produce a large number of physiological and pharmacological effects such as effects on the gastrointestinal tract, the cardiovascular and respiratory system as well as the sensory and thermoregulation system.

These effects result principally from the specific action of capsaicinoids on primary afferent neurons of the C-fiber type. This provides the rationale for their use to treat some peripheral painful states, such as rheumatoid arthritis (Surh and Lee,1995)

In addition, capsaicinoids are powerful irritants, causing burn and pain at low concentrations on the skin and mucous membranes. Given orally, they induce an increase of salivation and gastric secretion, a rapid change of sensation, warm to intolerable burning, and gastrointestinal disorders depending on the dose (Govindarajan and Sathyanarayana, 1991).

Absorption, distribution, metabolism and excretion

Capsaicinoids, when administered to rats intragastrically are readily absorbed and metabolized to a great extent in the liver before reaching the general circulation and extra hepatic organs (Donnerer et al., 1990). In vitro and in vivo studies have shown that capsaicinoids are metabolized by different pathways: (1) hydrolysis of the acid-amide-bond and oxidative deamination of the formed vanillylamine, (2) hydroxylation of the vanillyl ring, possibly via epoxidation, (3) one electron oxidation of the ring hydroxyl forming phenoxy radicals and capsaicinoid dimers, (4) oxidation at the terminal carbon of the side chain (Surh and Lee, 1995). Within 48 hrs after oral administration of dihydrocapsaicin to male rats, 8.7% of the dose were excreted unchanged in urine and 10% in faeces. Metabolites found in urine were vanillylamine (4.7%), vanillin (4.6%) vanillyl alcohol (37.6%) and vanillic acid (19.2%) in free form or as glucuronides (Kawada and Iwai, 1985).

Based on results of Miller et al. (1983), who demonstrated the covalent binding of dihydrocapsaicin to hepatic microsomal proteins, the formation of electrophilic intermediates (arene epoxides, phenoxy radicals or quinone type derivatives formed after O-demethylation) and subsequent covalent binding to cellular macromolecules is discussed to play a role in the etiology of capsaicin-induced toxicity including mutagenicity and carcinogenicity (Surh and Lee, 1995).

Acute toxicity

The acute toxicity of capsaicin shows a large variation depending on the route of administration. In male mice, the LD 50 varies from 0.56 mg/kg bw (i.v.) to 60 – 75 mg/kg bw (in ethanol) and 190 (122 – 294) mg/kg bw (in dimethyl sulfoxide), following intragastric intubation. The possible cause of death was considered to be due to respiratory paralysis (Glinsukon et al. 1980). Intraduodenal and intragastric administration of 10% Capsicum as well as 0.014% capsaicin in 0.85% saline to male rats produced morphological damages in the duodenal mucosa (Nopanitaya and Nye, 1974).

Subacute/subchronic toxicity

A 4-week feeding study with groups of 5 male B6C3F1 mice with 0, 0.5, 1.0, 2.5, 5.0, 7.5, and 10% ground red chilli (Capsicum annuum) in the diet showed slight glycogen depletion and anisocytosis of hepatocytes in the 10% group. Other organs did not reveal any lesions.

General health, body weight and food intake were not adversely affected (Jang et al., 1992).

Groups of 10 – 14 rats were fed by stomach tube with 50 mg/kg bw/day capsaicin or 0.5 g/kg bw/day Capsicum extract for 10 - 60 days. There were significant reductions of growth, plasma urea, glucose, phospholipids, triglycerides, total cholesterol, free fatty acids, glutamic pyruvic transaminase, and alkaline phosphatase in both groups with a tendency for Capsicum treated animals to show more adverse effects. No gross pathological changes and no differences in organ weights from control values were observed at autopsy, only a slight hyperemia in the livers and reddening with increasing mucous materials in the gastric mucosa.

The organs, however, were not examined histopathologically (Monsereenusorn, 1983).

BALB/c mice received an alcoholic chilli extract in drinking water 5 days a week till 16 months of age (27 males, 25 µg capsaicin/week, equivalent to about 0.125 mg/kg bw/d) or on the tongue 2 days a week for 14 months (22 males without and 19 males with 1% atropin solution prior to application, 50 µg capsaicin/week, equivalent to about 0.25 mg/kg bw/d).

Compared with 40 untreated mice, the treated animals showed increased mortality and histopathological changes in liver, kidneys, stomach and tongue. The lesions in the liver observed in all treated mice were in the form of focal necrosis with inflammatory cells around, fatty changes and fibrosis (Agrawal and Bhide, 1987).

36 male Syrian hamsters received 20 µl alcoholic chilli extract with 50 µg capsaicin (equivalent to about 0.5 mg/kg bw/d) 5 days a week by cheek pouch application for 14 months. 30 untreated animals and 17 hamsters treated with 20 µl alcohol were used as controls. The animals treated with chilli extract had increased mortality and histopathological lesions in liver, kidneys, stomach and cheek pouch. The main lesions were liver cirrhosis, observed in 49 % of examined livers from exposed hamsters compared to 8 and 17 % in the control groups and glomeruli degeneration in 50% of examined kidneys of exposed animals compared to 8 and 0 % in the control groups, respectively (Agrawal and Bhide, 1988).

Capsaicin, administered intraperitoneally to adult male mice at doses of 0.4, 0.8 or 1.6 mg/kg bw/day on 5 consecutive days, did not induce significant alterations in epididymal weights, caudal sperm counts, testicular weights or testicular histology. In the sperm morphology assay, sperms at 1, 3, 5 and 7 weeks did not reveal any treatment-related increase in the incidence of sperm-head abnormalities (Muralidhara and Narasimhamurthy, 1988).

In a 13-week study performed to determine the maximum tolerated dose, groups of 10 male and 10 female B6C3F1 mice received a mixture of 64.5% capsaicin and 32.6% dihydrocapsaicin at those levels of 0, 0.0625, 0.125, 0.25, 0.5, and 1% in the diet. Significant reduction of food intake and body weight gain in all dose groups, especially in treated females, and significantly increased liver/body weight ratios of both sexes and renal toxicity (focal tubular dilatation) in the 1% treated males were observed (Akagi et al., 1998).

Capsaicin (purum) was administered at concentrations of 0.0625, 0.125, 0.25, 0.5 and 1% in the diet of groups of 4 male and 4 female Swiss albino mice for 35 days. When the animals died at an age of 62 – 126 weeks, one adenocarcinoma of the duodenum had developed at each dose level, except for the highest dose, while no such tumours occurred in a historical control group of 100 males and 100 females. There was no concurrent control group and the observed tumour incidence was not dose-related (Toth et al., 1984).

Chronic toxicity/carcinogenicity

15 out of 26 rats fed for seven months with 10% chillies in a semisynthetic diet containing ardein, a purified protein of the ground nut, developed neoplastic changes in the liver (hepatomas, multiple cystic cholangiomas, solid adenomas or adenocarcinomas of the bile duct). Although no tumour developed in rats fed the basic diet without chillies, the authors stress, that it cannot be said whether chillies have a specific carcinogenic effect or whether a deficiency in the diet aggravated by a non-specific irritant caused the tumours (Hoch-Ligeti, 1951).

Capsaicin (capsaicin 65%, dihydro- 31%, nordihydro- 0.9%, homo- 1%, homodihydro- 0.6%, nor- 0.5%, nornor- 0.3%), administered in a semisynthetic diet at 0.03125% to 50 male and 50 female Swiss albino mice for their life span from 6 weeks of age, induced benign polypoid adenomas of the caecum in 22% of females (p <0.05) and 14% of males, compared to 8% in the untreated female and male controls (incidence of historical controls not given). The survival rate was not substantially altered (Toth and Gannet, 1992).

Groups of 50 male and 50 female B6C3F1 mice were given 0, 0.025, 0.083, and 0.25 % capsaicinoid mixture (64% capsaicin and 32.6% dihydrocapsaicin) in the diet for 79 weeks, equivalent to daily doses of up to 220 and 200 mg/kg bw in males and females, respectively. In all dose groups, food intake was significantly reduced, in females also the body weight gain and in males the liver/body weight ratio. No evidence of carcinogenicity was found. Renal cell adenomas developed only in one male mouse of the 0.025 and 0.25% groups. (Akagi et al., 1998).

A number of studies have shown that capsaicin or chilli extract can act as tumour promoters (Surh and Lee, 1995 and 1996). Thus, capsaicin (0.002% in drinking water for 6 weeks) has been reported to act as a promoter for the development of diethylnitrosamine-initiated enzyme-altered foci in the liver of male rats (Jang and Kim, 1988). Chilli extract has also been shown to have a promoting effect on the development of stomach and liver tumours in BALB/c mice initiated by methyl-acetoxy methylnitrosamine and benzene hexachloride, respectively (Agrawal et.al., 1986). In another study, rats fed diets containing hot chilli pepper showed slightly higher incidence of N-methyl-N-nitrosoguanidine-induced gastric cancer (Kim et al., 1985).

On the other side, capsaicin has been suggested to exert chemoprotective effects through modulation of metabolism of carcinogens and their interaction with target cell DNA (Surh and Lee, 1995 and 1996).

Genotoxicity

Capsaicin (purum) was found to be mutagenic in Salmonella typhimurium strain TA 98 in the presence of Aroclor induced rat liver S9 fraction (Toth et al., 1984), whereas another study in which S9 from phenobarbital-induced rats was used for metabolic activation was negative (Buchanan et al., 1981). Capsaicin containing 20% dihydrocapsaicin exhibited mutagenicity in Salmonella strains TA 98, TA 100 and TA 1535 in the presence of S9 mixture from Aroclor-induced rats. An alcoholic chilli extract was mutagenic only in strain TA 98 (Nagabhushan and Bhide, 1985 and 1986). Capsicum pepper oleoresin was reported to have mutagenic activity in Salmonella strains SD 1018 and SD 7823 without metabolic activation (Damhoeri et al., 1985). In addition, also a modified SOS microplate assay indicated a genotoxic activity of capsaicin (Venkat et al., 1995).

Capsaicin containing 20% dihydrocapsaicin and alcoholic chilli extract failed to induce 8- azaguanine resistant mutants in Chinese hamster V79 cells with and without metabolic activation by S9 from Aroclor-induced rats (Nagabhushan and Bhide, 1985). On the other side, synthetic capsaicin, dihydrocapsaicin and a crude mixture of capsaicinoides from Capsicum frutescens activated with hamster hepatocytes were mutagenic in the V 79 assay measured by resistance to ouabain and 6-thioguanine (Lawson and Gannet, 1989).

The results of the comet assay and a DNA fragmentation assay show that capsaicin is able to induce DNA damage in human neuroblastoma cells (Richeux et al., 1999). Capsaicin also induced DNA strand breakage with calf thymus and plasmid DNA in the presence of Cu (II) (Singh et al., 2001).

Capsaicin containing 20% dihydrocapsaicin induced micronuclei in polychromatic erythrocytes in the mouse-bone-marrow assay at 7.5 mg/kg i.p. (Nagabhushan and Bhide, 1985). It also produced a significant increase of micronucleated normochromatic erythrocytes in the peripheral blood and SCEs in bone marrow cells of male mice at 1.46 and 1.94 mg/kg i.p. (Diaz Barriga Arceo, 1995). A fraction of an alcoholic extract from the fruits of Capsicum frutescens, containing 3-acetamido-2-methyltetradecane as major component, has been found positive in the mouse-bone-marrow micronucleus assay after i.p. administration (Villasenor and Ocampo, 1994 and 1995). Dominant-lethal mutations in mice were not induced by capsaicin (Muralidhara and Narasimhamurthy, 1988).

Furthermore, capsaicin inhibited DNA biosynthesis in the testes of Swiss mice injected intraperitoneally (Nagabhushan and Bhide, 1985).

Some other studies cannot be evaluated, because important experimental details have not been published.

Reproductive and developmental toxicity

No data available

Human data

In a case-control study in Mexico-City which included 220 cases of gastric cancer and 752 controls randomly selected from the general population, chilli pepper consumers were at a 5.5 fold greater risk for gastric cancer than non-consumers. Persons who rated themselves as heavy consumers of chilli peppers were even at a 17 fold greater risk. However, when chilli pepper consumption was measured as frequency per day, a significant dose response relationship was not observed (Lopez-Carrillo et al., 1994).

In another case-control study in India, red chilli powder was found to be a risk factor for cancer of the oral cavity, pharynx, esophagus, and larynx (2- to 3-fold risk with a doseresponse relationship) compared with population controls, but not with hospital controls (Notani and Jayant, 1987).

In an Italian case-control study, chilli was briefly mentioned as being protective against stomach cancer (Buiatti et al., 1989). Chilli peppers, however, are not heavily consumed in Northern Italy, where this study was conducted, and it is possible that chilli consumption was correlated with other protecting spices such as onions and garlic that are more heavily consumed in Italy (comment from Lopez-Carrillo et al., 1994).

Summary of hazard identification/characterisation

Capsaicin, capsaicinoid mixtures, chillies and chilli extracts have been tested toxicologically by oral administration to mice, rats and hamsters. Some of these studies indicated a carcinogenic potential of capsaicin. These studies are regarded, however, as limited. A more recent carcinogenicity study did not show carcinogenic effects in mice. In humans, however, high consumption of chillies has been reported to be a risk factor for cancer of the upper gastrointestinal tract, possibly due to the irritating effect of capsaicinoids.

Genotoxic effects of capsaicin and capsaicinoid mixtures have been shown in vitro and in vivo.

Risk characterisation

The Committee concluded that the available data did not allow it to establish a safe exposure level for capsaicinoids in food.

The human intake of capsaicinoids in India, Thailand and Mexico, where capsicum spices are heavily consumed, has been estimated to be 25 – 200 mg/day. The high consumption of chillies in Mexico and India was reported to be associated with cancer of the upper digestive tract. In contrast, the maximum daily intake from mild chillies and paprika in Europe was roughly estimated to be 1.5 mg/day. In the one study conducted in Europe, no increase in the incidence of gastric cancer was found in association with occasional and lower intakes of chillies.

References

Agrawal, R. C., Wiessler, M., Heckers, E., Bhide, S. V., 1986. Tumour-promoting effect of chilli extract in balb/c mice. Int. J. Cancer, 38, 689-695.

Agrawal, R. C., Bhide, S. V., 1987. Biological studies on carcinogenicity of chillies in balb/c mice. Indian J Med. Res., 86, 391-396.

Agrawal, R. C., Bhide, S. V., 1988. Histopathological studies on toxicity of Chilli (Capsaicin) in Syrian golden hamsters. Indian J. Experim. Biol., 26, 377-382.

Akagi, A., Sano, N., Uehara, H., Minami, T., Otsuka, H., Izumi, K., 1998. Noncarcinogenicity of capsaicinoids in B6C3F1 mice. Food Chem. Toxicol., 36, 1065-1071.

Buchanan, R. L., Goldstein, S., Budroe, J. D., 1981. Examination of chili pepper and nutmeg oleoresins using the salmonella/mammalian microsome mutagenicity assay. J. Food Sci., 47, 330-333.

Buiatti, E., Palli, D., Decarli, A., Amadori, D., Avelini, C., Bianchi, S., Biserni, R., Cipriani F., Cocco, P., Giacosa, A. Marubini, E., Puntoni, R., Vindigni, C., Fraumeni, J., Jr., Blot, W., 1989. A case-control study of gastric cancer and diet in Italy. Int. J. Cancer, 44, 611-616.

Council of Europe, 2001. Committee of experts on flavouring substances. Datasheet on capsaicin.

CREDOC/OCA (Observatoire des Consommations Alimentaires) 1998. Estimation des niveaux d’ingestion de substances aromatisantes Safrole, Estragole, Coumarine et Capsaicine. Note technique No. 98.25

Damhoeri, A., Hosono, A., Itoh, A., Matsuyama, A., 1985. In vitro mutagenicity tests on capsicum pepper, shallot and nutmeg oleoresins. Agric. Biol. Chem., 49 (5), 1519-1520.

Diaz Barriga Arceo, S., Madrigal-Bujaidar, E., Calderon Montellano, E., Ramirez Herrera, L.,

Diaz Garcia, B. D., 1995. Genotoxic effects produced by capsaicin in mouse during subchronic treatment. Mutat. Res., 345, 105-109.

Donnerer, J., Amann, R., Schuligoi, R., Lembeck, F., 1990. Absorption and metabolism of capsaicinoids following intragastric administration in rats. Naunyn-Schmiedeberg’s Arch. Pharmacol., 342, 357-361.

EC, 1999. Commission Decision 1999/217/EC adopting a register of flavouring substances used in or on foodstuffs drawn up in application of Regulation (EC) N° 2232/96 of the European Parliament and of the Council of 28 October 1996. Official Journal of the European Communities, 27.3.1999, L 84/1-137.

EC, 2002. Commission Decision 2002/113/EC amending Decision 1999/217/EC as regards the register of flavouring substances used in or on foodstuffs. Official Journal of the European Communities, 20.2.2002, L 49/1.

Glinsukon, T., Stitmunnaithum, V., Toskulkao, C., Buranawuti, T., Tangkrisanavinont, V., 1980. Acute toxicity of capsaicin in several animal species. Toxicon, 18, 215-220.

Govindarajan, V.S., and Sathyanarayana, M.N., 1991. Capsicum-production, technology, chemistry, and quality. Part V. Impact on Physiology, Pharmacology, Nutrition, and Metabolism; Structure, Pungency, Pain, and Desensitization Sequences. Crit. Rev. Food Sci. Nutr., 29 (6), 435-473.

Hoch-Ligeti, C.,1951. Production of liver tumours by dietary means: Effect of feeding chillies to rats. Acta unio internationalis contra cancrum, 7, 606-611.

Jang, J. J., Kim, S. H., Yun, T.K., 1992. A 4-week feeding study of ground red chilli (Capsicum annuum) in male B6C3F1 mice. Food Chem. Toxicol., 30, 783-787.

Jang, J.J., Kim, S.H., 1988. The promoting effect of capsaicin on the development of diethylnitrosamine-induced enzyme altered hepatic foci in male Sprague-Dawley rats. J.

Korean Cancer Assoc., 20, 1-7.

Kawada, T., Iwai, K., 1985. In vivo and in vitro metabolism of dihydrocapsaicin, a pungent principle of hot pepper, in rats. Agric. Biol. Chem., 49 (2), 441-448.

Kim, J. P., Park, J. G., Lee, M. D., Han, M. D., Park, S. T., Lee, B. H., Jung, S. E., 1985. Cocarcinogenic effects of several Korean foods on gastric cancer induced by N-methyl-N´-nitro-N-nitrosoguanidine in rats. Jap. J. Surg., 15, 427-437.

Lawson, T., Gannett, P., 1989. The mutagenicity of capsaicin and dihydrocapsaicin in V79 cells. Cancer Lett., 48, 109-113.

Lopez-Carrillo, L., Avila, H. M., Dubrow, R., 1994. Chili pepper consumption and gastric cancer in Mexico: A case-control study. Am. J. Epidemiol., 139 (3), 263-271.

Lopez-Hernandez, J., Oruna-Concha, M. J., Simal-Lozano, J., Gonzales-Castro, M. J.,

Vazquez-Blanco, M. E., 1996. Determination of capsaicin and dihydrocapsaicin in cayenne pepper and padron peppers by HPLC. Deutsche Lebensmittel-Rundschau, 92, 393-395.

Miller, M. S., Brendel, K., Burks, T. F., Sipes, I. G., 1983. Interaction of capsaicinoids with drug-metabolizing systems. Relationship to toxicity. Biochem. Pharmacol., 32 (3), 547-551.

Monsereenusorn, Y., 1983. Subchronic toxicity studies of capsaicin and capsicum in rats. Res. Commun. Chem. Pathol. Pharmacol., 41 (1), 95-110.

Muralidhara, and Narasimhamurthy, K., 1988. Non-mutagenicity of capsaicin in albino mice. Food Chem. Toxicol., 26 (11/12), 955-958.

Nagabhushan, M., Bhide, S. V., 1985. Mutagenicity of chili extract and capsaicin in shortterm tests. Environ. Mutagen., 7, 881-888.

Nagabhushan, M., Bhide, S. V., 1986. Nonmutagenicity of curcumin and its antimutagenic action versus chili and Capsaicin. Nutr. Cancer, 8 (3), 201-210.

Nopanitaya, W., Nye, S. W., 1974. Duodenal mucosal response to the pungent principle of hot pepper (capsaicin) in the rat: Light and electron microscopic study. Toxicol. Appl. Pharmacol., 30, 149-161.

Notani P. N., Jayant, K., 1987. Role of diet in upper aerodigestive tract cancers. Nutr. Cancer, 10 (1/2), 103-113.

Parrish, M., 1996. Liquid chromatographic method of determining capsaicinoids in capsicums and their extractives: Collaborative study. J. Assoc. Off. Anal. Chem. Intern., 79 (3), 738-745.

Richeux, F., Cascante, M., Ennamany, R., Saboureau, D., Creppy, E. E., 1999. Cytotoxicity and genotoxicity of capsaicin in human neuroblastoma cells SHSY-5Y. Arch. Toxicol., 73, 403-409.

Singh, S., Asad A. F., Ahmad, A., Khan, N. U., Hadi, S. M., 2001. Oxidative DNA damage by capsaicin and dihydrocapsaicin in the presence of Cu(II). Cancer Lett., 169, 139-146.

Surh, Y.-J., Lee, S. S., 1995. Capsaicin, a double-edged sword: Toxicity, metabolism, and chemopreventive potential. Life Sci., 56 (22), 1845-1855.

Surh, Y.-J., Lee, S. S., 1996. Capsaicin in hot chili pepper: Carcinogen, co-carcinogen or anticarcinogen? Food Chem. Toxicol., 34 (3), 313-316.

Thomas, B. V., Schreiber, A. A., Weisskopf, C. P., 1998. Simple method for quantitation of capsaicinoids in peppers using capillary gas chromatography. J. Agric. Food Chem., 46, 2655-2663.

Toth, B., Gannett, P.,1992. Carcinogenicity of lifelong administration of capsaicin of hot pepper in mice. In vivo, 6, 59-64.

Toth, B., Rogan, E., Walker, B., 1984. Tumorigenicity and mutagenicity studies with capsaicin of hot peppers. Anticancer Res., 4, 117-120.

Venkat, J. A., Shami, S., Davis, K., Nayak, M., Plimmer, J. R., Pfeil, R. Nair, P. P., 1995. Relative genotoxic activities of pesticides evaluated by a modified SOS microplate assay. Environ. Mol. Mutagen., 25, 67-76.

Villasenor I. M., De Ocampo 1994. Clastogenicity of red pepper (Capsicum frutescens L.) extracts. Mutat. Res., 312, 151-155.

Villasenor I. M., De Ocampo, E. J., Bremner J. B., 1995. Genotoxic acetamide(s) from Capsicum frutescens fruits. Natural Prod. Lett., 6, 247-253.