capscicum 001

8/6/2019 Capscicum 001

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EL AJI

LA ESPECIA DEL NUEVO MUNDO

PROPIEDADES DE LA HORTALIZA PERUANA

INTRODUCCION

El picante ttulo no deja terreno sin explorar. Los origenes, el paso a travs de la historia, laspropiedades condimenticias, medicinales y socializantes, las mltiples especies, la composicinqumica, el mecanismo del dolor, as como las actitudes culturales y sociales que se dan en el Pery el mundo alrededor de esta planta.

El gnero Capsicum, que incluye entre 20 a 30 especies, tiene su centro de origen en las regionestropicales y subtropicales de Amrica, probablemente en el rea Bolivia-Per, donde se hanencontrado semillas de formas ancestrales de ms de 7.000 aos, y desde donde se habradiseminado a toda Amrica. Al menos cinco de sus especies son cultivadas en mayor o menorgrado pero, a nivel mundial al igual que en Per, casi la totalidad de la produccin de aj y pimientoest dada por una sola especie, Capsicum annuum. Esto tiende a confundir porque a partir deesta especie se generan dos productos distintos para el consumidor: aj (del arawak axi) o frutopicante, y pimiento (de pimienta, por equivocacin de C. Coln) o frutos no picantes. Los trminosespaoles pimentn y paprika deben reservarse para el producto seco y molido de la especie.

Es necesario destacar que existen otras especies del gnero cuyo fruto o producto tambin esdenominado aj, y solo tienden a hacer ms confusa la situacin. Estas especies de inters mspuntual son Capsicum chinense, cuyo cultivar "Habanero" produce el aj ms picante que se

conoce, Capsicum frutescens, cuyo cultivar "Tabasco" es muy usado para la elaboracin de salsapicante y pickles, Capsicum baccatum, cuyo producto es conocido como aj andino y esampliamente cultivado en las zonas altiplnicas, y Capsicum pubescens, cuyo cultivar "Rocoto"(Manzano y Siete Caldos son sinnimos) es muy apreciado por su sabor y picantez en diversasregiones de Amrica.


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Capsicum chinense Capsicum frutescens Capsicum baccatum

Capsicum pubescens

Despus del descubrimiento de Amrica todas estas especies, principalmente Capsicum annuum,han sido llevadas a distintas regiones del mundo y rpidamente han pasado a ser la principal"especia" o condimento de comidas tpicas de muchos pases, por lo que su cultivo, aunque

generalmente reducido en superficie, se encuentra ampliamente extendido, siendo Per, China,Estados Unidos y Mxico los principales productores a nivel mundial.


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"El enamoramiento de los peruanos con el aj es largo eininterrumpido" dice Cabieses. Cermicas y textilesprehispnicos retratan al ardiente condimento como unaplanta de gran importancia no slo como alimento sino encontextos mgicos y religiosos.

Ucho, el nombre de uno los Hermanos Ayar, la dinastafundadora del imperio incaico, significa aj. Unido a Cachi:sal; Auca: guerrero; y Manco el jefe fundador, conformanlos factores que fueron esenciales para la fundacin delgran imperio

Sal y aj eran entonces los acompaantes obligatorios detodo alimento, como lo siguen siendo hoy. El aj es elcondimento ms generalizado en el mundo entero. Supresentacin natural vara en tamao, forma, color ycalidad. Se usa fresco o procesado en diversas formas,seco, ahumado, entero, picado o molido; congelado,enlatado o envasado; con vinagre o sin l, en salmuera o

en una variedad impresionante de salsas y preparados.

Aunque en otros pases existan diferentes vocablos parareferirse a las distintas variedades en el Per se utiliza lapalabra aj para referirse a todo fruto clasificado dentro delgnero capsicum.

Ajamarillo

Todas las especies de aj son originaria de America y en la colonia los ajs fueron llevados aespaa, desde donde se dispersaron a toda Europa y de all al resto del mundo. Es ms, algunasvariedades de aj que llegaron a Estados Unidos fueron introducida por los inmigrantes europeos,en ves de haber llegado directamente de sudamrica o Mxico.

En el Per, el cultivo del aj esta muy difundido dado que el rea de cultivo que ocupa nosrepresenta del 6 al 7% del rea total cultivada de hortalizas (Vallejo,1974).En el mbito mundial se destinan 986,00 ha. para su cultivo, totalizando una produccin de7'205,000 TM con un rendimiento promedio de 7,308 Kg./Ha.. En el Per se cultivan ms de 2,000Ha. con una produccin promedio de 5,532 Kg./Ha.. Las zonas donde se producen en mayorescala son los valles de Lima, Chincha, Caete, Tacna, Oxapampa y Cerro de Pasco (Ortiz, 1983)En el pas se cultivan diferentes variedades de aj, en las tres regiones, donde existen muchasreas agrcolas aptas para la produccin comercial se realiza como cultivo anual debido a la fuerteincidencia de hongos que maltratan a las plantas (Capsicum pubescens), existiendo tambin enla Sierra, pero en menor escala (Corrales,1980)

Actualmente por sus propiedades pungentes (picante) y aromticas se le utiliza seco, base para lassalsas y pastas, estimulante digestivo, sazonador, como antioxidante en carnes y otros; lo quedemuestra ser un recurso de amplsimo rango de aprovechamiento para su industrializacin ymenor prdida con relacin al fruto fresco.

El Concejo Internacional de Recursos Fitogenticos con sede en Costa Rica, desde 1979 hareconocido a nivel mundial la importancia socio econmica y cientfica del gnero Capsicum, alcual pertenece el rocoto, siendo considerado dentro de los recursos fitogenticos de primeraprioridad, recomendando su recoleccin, evaluacin en la estabilizacin y conservacin(Ortiz,1983)

DESCRIPCION DEL ROCOTO


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El cultivo del rocoto se remontadesde pocas pre-incas hastala actualidad, es el principalcondimento de nuestrascomidas, usado principalmentepor su sabor pungente (picante)

sin que muchas veces se tengaidea del valor alimenticio,especficamente vitamnico y elpapel importante que por ellopodra estar desempeando enla dieta diaria nacional, ancuando sea usado en pequeasproporciones (Vallejo 1968).El nombre cientfico Capsicumpubescens, su nombrecomercial es rocotoperteneciendo a la familiaSolanceas, generalmente laszonas de produccin son los

valles andinos, la poca desiembra es todo el ao teniendocomo mbito un climatemplado, favoreciendo unatemperatura ptima que fluctaentre los 18 a 20 C con unahumedad relativa baja.

La cosecha se realizar cuando presente una coloracin de fruto verde o maduro. Con buenamanipulacin agrcola se llega a rendimientos de 200,000 frutos/Ha. (Orbegoso,1954).

En cuanto a la duracin del poder germinativo de la semilla de aj es necesario utilizar semilla de

un ao o mximo de tres, conservada 7 das en lugares frescos y ventilados por 20 das a unatemperatura 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, tamao y color de los frutos, es muy variable segn sus caractersticasgenticas; el tamao en cuanto a la variedad es inconstante, al iniciarse la cosecha pueden ser detamao notablemente mayor que al trmino de sta(Velasco,1971).

ORIGEN DE LA HORTALIZA

Lippert,(1926) seala que el origen del gnero Capsicumcorresponde al nuevo mundo, tenindosereferencias de bayas secas encontradas en tumbas del Per con antigedad de 2,000 aos.Vavilov seala que el gnero Capsicum es de origen centro americano, correspondiendo suubicacin al Centro de Origen VII (Mxico y Centro Amrica) . El Per por albergar gran

variedad de especies tanto silvestres como cultivadas, es considerado como Centro de OrigenSecundario ya que cuenta con todos los recursos apropiados para su fertilidad y expectativas deabundante produccin.Orbegoso,(1954) menciona que el gnero Capsicum puede derivarse de la palabra CAPSA (Caja)teniendo como referencia la forma del fruto; mientras que Velasco(1971) seala que el nombreproviene de la palabra CAPTO (morder) por su naturaleza picante.Len, (1968) describe a las plantas del gnero Capsicum como herbcea o arbustiva, de troncoleoso y ramificacin dicatmica, con hojas alternadas, lisas y brillantes, excepto en C. pubesces,que presenta hojas rugosas pubescentes.


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CLASIFICACION SISTEMATICA QUEREPORTA ALVISTUR(1975)

Divisin : Fanergamas o Spermofitas(Strasburger 1963) o Antofitas (Coronado1960)

Sub divisin : AngiospermasClase :DicotiledoneasSub clase : Simptalas ogamoptalas(Bayluy,1928)Orden : TumiflorasSub Orden : SolanineasFamilia : SolanceasTribu : SolanineasGnero : CapsicumEspecie : Capsicum pubescens R y PNombre Comn : Rocoto

COMPOSICION DE LA HORTALIZA

Anlisis dietticos practicados por el Departamento de Nutricin del Ministerio de Salud delPer(1978) le asignan los siguientes valores:

Por 100 gr., de peso neto Mnimo Mximo

Agua 20.7 gr. 93.1 gr.

Hidratos de Carbono 5.3 gr 63.8 gr.

Protenas 0.8 gr 6.7 gr.

Extracto etreo 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

Fsforo 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. ascrbico 14.4 mg 157.5 mg

Caloras 23 233

Capcisina 150 mg 335 mg por 10 gr./peso

ESPECIES CULTIVADAS ENEL PERU

Las especies del gnero Capsicum, que incluye todas las variedades de aj, tanto dulces (pimiento)como picantes (rocoto), han sufrido diversas modificaciones en su clasificacin siendo la msreciente, la aprobada en la Reunin de Consulta sobre recursos fitogenticos de Capsicum,

en Costa Rica el ao 1980. En ella se determin que son cinco las especies cultivadas :


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

C. annuum (Mex y EEUU) .................. Dulce (pimiento)...picante(Chile)C. chinense(Arequipa, La Molina) ........ Aj panca, limoC. frutescens (Piura) .......................... Aj arnaucho, monoC. baccatum (La Libertad) .................. Aj escabeche o mirasol

C. pubescens (Lima)............................Rocoto

BIBLIOGRAFIA:

-,Ch.C.(1962) "Composicin de los Alimentos Peruanos" Instituto de Nutricin tercera edicin Lima-Per.-Chiappe,L (1960) "Estudio comparativo de diversas variedades de aj" Tesis de Grado. LM.-Corrales,N.(1961) "El cultivo del Aj en el Per" Estacin Experimental de Agricultura. La Molina.-Delgado,D.F (1988) "Cultivos Hortcolas datos bsicos" Edi-Agraria Universidad.-ITINTEC norma tcnica :209.238-1986 "Salsa de Aj"209.035-1970 "Pimentn"209.070-1970 "Vinagre"

209.132-1986 "Determinacin de Ceniza"209.102-1975 "Especies y Condimentos"203.071-1975 "Productos elaborados a partir de frutas y otros vegetales.-Orbegoso,A(1954) "Resea del Cultivo, identificacin botnica y comparativo de rendimiento enfresco de variedades de aj Escuela Nacional de Agricultura. La Molina.-Ortiz,R(1983) Utilizacin de descriptores en la caracterizacin de lneas de Capsicum.UNA-Velasco,F.(1971) "Recoleccin y descripcin de muestras del G. Capsicum en la provincia deSatipo (Junin) y San Miguel (Cajamarca).UNA.

Chemical characterisation

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


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Synonyms: 8-Methylnon-6-enoyl-4-hydroxy-3-methoxybenzylamide; trans-8- methyl-N-

vanillyl-6-nonenamide; Isodecenoicacid vanillylamide

FL No: 16.014

CAS No: 404-86-4

FEMA No: 3404

CoE No: 2299

EINECS: 206-969-8

Structure:

CapsaicininCapsicumpreparationsisalwaysaccompanied by othercapsaicinoids: mainlydihydrocapsaicin, but also small amounts ofnordihydro-, homo-, homodihydro-,nor-,and

nornorcapsaicin. The capsaicinoidspresent in the Capsicum fruit are predominantlycapsaicinand dihydrocapsaicin, makingup 80 to 90%. The ratio ofcapsaicin to

dihydrocapsaicinisgenerally around 1:1 and 2:1 (Govindarajanand Sathyanarayana,

1991).

Exposure assessment

Capsaicinoidsare mainly ingested asnaturally occurringpungency-producingcomponents

ofcapsicum spices (chilli,cayenne pepper, red pepper). They typically range from 0.1 mg/ginchillipepper to 2.5 mg/gin red pepperand 60 mg/gin 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 (Thomaset al., 1998). Cayenne pepper

samples had meancapsaicinand dihydrocapsaicincontents of 1.32 and 0.83 mg/g dryweight, respectively (Lopez-Hernandez, 1996).

The consumption ofcapsicum spices was reported to be 2.5 g/person/day in India, 5g/person/day in Thailand (Monsereenusorn, 1983) and 20 g/person (one chillipepper) per

day in Mexico (Lopez-Carrillo, 1994). Assumingacontent ofcapsaicinoidsin these spicesofabout 1%, the daily intake ofcapsaicinoidsin these countries has been estimated to be 25


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- 200 mg/person/day orin the case ofaperson with 50 kg body weight 0.5 4 mg/kg

bw/day (Council of Europe, 2001).

The maximum daily intake ofcapsaicinin the U.S. and Europe from mild chilliesandpaprika was roughly estimated to be 0.025 mg/kg bw (Govindarajanand Sathyanarayana,

1991), equivalent to 1.5 mg/person/day. According to a recent estimation, the meanandmaximum intake ofcapsaicin from industriallyprepared food productscontaining the

recommended general limit of 5 ppm would be 0.77 and 2.64 mg/day, respectively(CREDOC/OCA, 1998).

Hazard identification/characterisation

Capsaicinand other members of the group ofcapsaicinoidsproduce a large number ofphysiological and pharmacological effectssuch as effects on the gastrointestinal tract, the

cardiovascularand respiratory system as well as the sensory and thermoregulationsystem.

These effects result principally from the specificaction ofcapsaicinoids onprimary afferentneurons of the C-fiber type. Thisprovides the rationale for theiruse to treat some peripheralpainful states,such as rheumatoid arthritis (Surh and Lee,1995)

Inaddition,capsaicinoidsare powerful irritants,causing burnand painat low

concentrations on the skinand mucous membranes. Given orally, they induce anincreaseofsalivationand gastricsecretion,a rapid change ofsensation, warm to intolerable burning,

and gastrointestinal disorders depending on the dose (Govindarajanand Sathyanarayana,1991).

Absorption, distribution, metabolism and excretion

Capsaicinoids, whenadministered to ratsintragastrically are readily absorbed andmetabolized to agreat extent in the liver before reaching the general circulationand extra

hepatic organs (Donnereret al., 1990). In vitro and in vivo studies have shown thatcapsaicinoidsare metabolized by different pathways: (1) hydrolysis of the acid-amide-bond

and oxidative deamination of the formed vanillylamine, (2) hydroxylation of the vanillylring,possibly via epoxidation, (3) one electron oxidation of the ring hydroxyl forming

phenoxy radicalsand capsaicinoid dimers, (4) oxidationat the terminal carbon of the sidechain (Surh and Lee, 1995). Within 48 hrsafter oral administration of dihydrocapsaicin to

male rats, 8.7% of the dose were excreted unchanged inurine and 10% in faeces.Metabolites found inurine were vanillylamine (4.7%), vanillin (4.6%) vanillyl alcohol

(37.6%) and vanillicacid (19.2%) in free form orasglucuronides (Kawadaand Iwai,1985).

Based on results of Milleret al. (1983), who demonstrated the covalent binding of

dihydrocapsaicin to hepatic microsomal proteins, the formation of electrophilicintermediates (arene epoxides,phenoxy radicals or quinone type derivatives formed after

O-demethylation) and subsequent covalent binding to cellular macromoleculesis discussedto play a role in the etiology ofcapsaicin-induced toxicity including mutagenicity and

carcinogenicity (Surh and Lee, 1995).


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Acute toxicity

The acute toxicity ofcapsaicinshowsa 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/kgbw (in ethanol) and 190 (122 294) mg/kg bw (in dimethyl sulfoxide), following

intragastricintubation. The possible cause of death wasconsidered to be due to respiratoryparalysis (Glinsukonet al. 1980). Intraduodenal and intragastricadministration of 10%

Capsicum as well as 0.014% capsaicinin 0.85% saline to male ratsproducedmorphological damagesin the duodenal mucosa (Nopanitayaand Nye, 1974).

Subacute/subchronic toxicity

A 4-weekfeedingstudy 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 hepatocytesin the 10% group. Other organs did not reveal any lesions.

General health, body weight and food intake were not adversely affected (Janget 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 ofgrowth,plasmaurea,glucose,phospholipids, triglycerides, total cholesterol, free fatty

acids,glutamicpyruvic transaminase,and alkaline phosphatase in both groups with atendency forCapsicum treated animals to show more adverse effects. No grosspathological

changesand no differencesin organ weights from control values were observed at autopsy,only aslight hyperemiain the liversand reddening with increasing mucous materialsin the

gastric mucosa.

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

BALB/c mice received analcoholicchilli extract in drinking water 5 daysa weektill 16

months ofage (27 males, 25 gcapsaicin/week, equivalent to about 0.125 mg/kg bw/d) oron the tongue 2 daysa weekfor 14 months (22 males without and 19 males with 1%

atropinsolutionprior to application, 50 gcapsaicin/week, equivalent to about 0.25 mg/kgbw/d).

Compared with 40 untreated mice, the treated animalsshowed increased mortality and

histopathological changesin liver,kidneys,stomach and tongue. The lesionsin the liverobserved inall treated mice were in the form of focal necrosis with inflammatory cells

around, fatty changesand fibrosis (Agrawal and Bhide, 1987).

36 male Syrian hamsters received 20 l alcoholicchilli extract with 50 gcapsaicin(equivalent to about 0.5 mg/kg bw/d) 5 daysa weekby cheekpouch application for 14

months. 30 untreated animalsand 17 hamsters treated with 20 l alcohol were used ascontrols. The animals treated with chilli extract had increased mortality and

histopathological lesionsin liver,kidneys,stomach and cheekpouch. The main lesionswere livercirrhosis, observed in 49 % of examined livers from exposed hamsterscompared


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to 8 and 17 % in the control groupsand glomeruli degenerationin 50% of examined

kidneys of exposed animalscompared 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 alterationsin epididymalweights,caudal sperm counts, testicular weights or testicular histology. In the sperm

morphology assay,spermsat 1, 3, 5 and 7 weeks did not reveal any treatment-relatedincrease in the incidence ofsperm-head abnormalities (Muralidharaand Narasimhamurthy,

1988).

Ina 13-weekstudyperformed to determine the maximum tolerated dose,groups of 10 male

and 10 female B6C3F1 mice received a mixture of 64.5% capsaicinand 32.6%dihydrocapsaicinat 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 gaininall dose groups, especially intreated females,and significantly increased liver/body weight ratios of both sexesand renal

toxicity (focal tubular dilatation) in the 1% treated males were observed (Akagiet al.,1998).

Capsaicin (purum) wasadministered at concentrations of 0.0625, 0.125, 0.25, 0.5 and 1%

in the diet ofgroups of 4 male and 4 female Swissalbino mice for 35 days. When theanimals died at anage of 62 126 weeks, one adenocarcinoma of the duodenum had

developed at each dose level, except for the highest dose, while no such tumours occurredina historical control group of 100 malesand 100 females. There wasno concurrent control

groupand the observed tumourincidence wasnot dose-related (Toth et al., 1984).

Chronic toxicity/carcinogenicity

15 out of 26 rats fed forseven months with 10% chilliesinasemisynthetic diet containing

ardein,apurified protein of the ground nut, developed neoplasticchangesin the liver(hepatomas, multiple cysticcholangiomas,solid adenomas oradenocarcinomas of the bile

duct). Although no tumour developed in rats fed the basic diet without chillies, the authorsstress, that it cannot be said whetherchillies have aspecificcarcinogenic effect or whether

a deficiency in the diet aggravated by anon-specificirritant 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 inasemisynthetic diet at 0.03125% to 50male and 50 female Swissalbino mice for their life span from 6 weeks ofage,induced

benignpolypoid adenomas of the caecum in 22% of females (p


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body weight gainand in males the liver/body weight ratio. No evidence ofcarcinogenicity

was found. Renal cell adenomas developed only in one male mouse of the 0.025 and 0.25%groups. (Akagiet al., 1998).

A number ofstudies have shown that capsaicin orchilli extract canact as tumourpromoters

(Surh and Lee, 1995 and 1996). Thus,capsaicin (0.002% in drinking water for 6 weeks) hasbeen reported to act asapromoter for the development of diethylnitrosamine-initiated

enzyme-altered fociin the liver of male rats (Jangand Kim, 1988). Chilli extract hasalsobeenshown to have apromoting effect on the development ofstomach and liver tumoursin

BALB/c mice initiated by methyl-acetoxy methylnitrosamine and benzene hexachloride,respectively (Agrawal et.al., 1986). Inanotherstudy, rats fed dietscontaining hot chillipeppershowed slightly higherincidence of N-methyl-N-nitrosoguanidine-induced gastric

cancer (Kim et al., 1985).

On the otherside,capsaicin has beensuggested to exert chemoprotective effects throughmodulation of metabolism ofcarcinogensand theirinteraction with target cell DNA (Surh

and Lee, 1995 and 1996).

Genotoxicity

Capsaicin (purum) was found to be mutagenicinSalmonella typhimurium strain TA 98 in

the presence of Aroclorinduced rat liver S9 fraction (Toth et al., 1984), whereasanotherstudy in which S9 fromphenobarbital-induced rats wasused for metabolicactivation was

negative (Buchananet al., 1981). Capsaicincontaining 20% dihydrocapsaicin exhibitedmutagenicity in Salmonellastrains TA 98, TA 100 and TA 1535 in the presence of S9

mixture from Aroclor-induced rats. Analcoholicchilli extract was mutagenic only instrainTA 98 (Nagabhushanand Bhide, 1985 and 1986). Capsicumpepper oleoresin was reported

to have mutagenicactivity in Salmonellastrains SD 1018 and SD 7823 without metabolicactivation (Damhoeriet al., 1985). Inaddition,also a modified SOS microplate assay

indicated agenotoxicactivity ofcapsaicin (Venkat et al., 1995).

Capsaicincontaining 20% dihydrocapsaicinand alcoholicchilli extract failed to induce 8-azaguanine resistant mutantsinChinese hamster V79 cells with and without metabolic

activation by S9 from Aroclor-induced rats (Nagabhushanand Bhide, 1985). On the otherside,syntheticcapsaicin, dihydrocapsaicinand acrude mixture ofcapsaicinoides from

Capsicum frutescens activated with hamster hepatocytes were mutagenicin the V 79 assaymeasured by resistance to ouabainand 6-thioguanine (Lawsonand Gannet, 1989).

The results of the comet assay and a DNA fragmentationassay show that capsaicinisable

to induce DNA damage in humanneuroblastomacells (Richeux et al., 1999). Capsaicinalso induced DNA strand breakage with calf thymusand plasmid DNA in the presence of

Cu (II) (Singh et al., 2001).

Capsaicincontaining 20% dihydrocapsaicininduced micronucleiinpolychromatic

erythrocytesin the mouse-bone-marrow assay at 7.5 mg/kgi.p. (Nagabhushanand Bhide,1985). It also produced asignificant increase of micronucleated normochromatic

erythrocytesin the peripheral blood and SCEsin bone marrow cells of male mice at 1.46


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and 1.94 mg/kgi.p. (Diaz Barriga Arceo, 1995). A fraction ofanalcoholic extract from the

fruits ofCapsicum frutescens,containing 3-acetamido-2-methyltetradecane as majorcomponent, has been found positive in the mouse-bone-marrow micronucleusassay after

i.p. administration (Villasenorand Ocampo, 1994 and 1995). Dominant-lethal mutationsinmice were not induced by capsaicin (Muralidharaand Narasimhamurthy, 1988).

Furthermore,capsaicininhibited DNA biosynthesisin the testes of Swiss mice injected

intraperitoneally (Nagabhushanand Bhide, 1985).

Some otherstudiescannot be evaluated, because important experimental details have not

beenpublished.

Reproductive and developmental toxicity

No dataavailable

Human data

Inacase-control study in Mexico-City which included 220 cases ofgastriccancerand 752

controls randomly selected from the generalpopulation,chillipepperconsumers were at a5.5 fold greater riskforgastriccancer thannon-consumers. Persons who rated themselves

as heavy consumers ofchillipeppers were evenat a 17 fold greater risk. However, whenchillipepperconsumption was measured as frequencyper day,asignificant dose response

relationship wasnot observed (Lopez-Carrillo et al., 1994).

Inanothercase-control study in India, red chillipowder was found to be a riskfactor for

cancer of the oral cavity,pharynx, esophagus,and larynx (2- to 3-fold riskwith adoseresponse relationship) compared with populationcontrols, but not with hospital

controls (Notaniand Jayant, 1987).

Inan Italiancase-control study,chilli was briefly mentioned as beingprotective againststomach cancer (Buiattiet al., 1989). Chillipeppers, however,are not heavily consumed in

Northern Italy, where thisstudy wasconducted,and it ispossible that chilliconsumptionwascorrelated with otherprotectingspicessuch as onionsand garlic that are more heavily

consumed in Italy (comment from Lopez-Carrillo et al., 1994).

Summary of hazard identification/characterisation

Capsaicin,capsaicinoid mixtures,chilliesand chilli extracts have been tested

toxicologically by oral administration to mice, ratsand hamsters. Some of these studiesindicated acarcinogenicpotential ofcapsaicin. These studiesare regarded, however,as

limited. A more recent carcinogenicity study did not show carcinogenic effectsin mice. Inhumans, however, high consumption ofchillies has been reported to be a riskfactor for

cancer of the uppergastrointestinal tract,possibly due to the irritating effect ofcapsaicinoids.


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Genotoxic effects ofcapsaicinand capsaicinoid mixtures have beenshownin vitro and in

vivo.

Risk characterisation

The Committee concluded that the available data did not allow it to establish asafeexposure level forcapsaicinoidsin food.

The humanintake ofcapsaicinoidsin India, Thailand and Mexico, where capsicum spicesare heavily consumed, has been estimated to be 25 200 mg/day. The high consumption of

chilliesin Mexico and India was reported to be associated with cancer of the upperdigestive tract. Incontrast, the maximum daily intake from mild chilliesand paprikain

Europe was roughly estimated to be 1.5 mg/day. In the one study conducted in Europe,noincrease in the incidence ofgastriccancer was found inassociation with occasional and

lowerintakes ofchillies.

References

Agrawal,R. C., Wiessler, M., Heckers, E., Bhide, S. V., 1986. Tumour-promoting effect of

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