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AUSTRALASIAN JOURNAL OF ECOTOXICOLOGY Vol. 12, pp. 129-134, 2006

Fenvalerate toxicity to fish Datta and Kaviraj

DIETARY ASCORBIC ACID SUPPLEMENTATION TO AMELIORATE CHRONIC TOXICITY OFFENVALERATE TO CLARIAS GARIEPINUS

Madhuban Datta (Bhattacharya)1,2and Anilava Kaviraj1*1 Department of Zoology, University of Kalyani, Kalyani-741235, West Bengal, India.2 Present address: Nabadwip Vidyasagar College, Nabadwip, Nadia, West Bengal, India.Manuscript received, 4/12/2006; accepted, 7/1/2007.

ABSTRACTSixty-day static renewal bioassays were conducted to evaluate the chronic toxicity of the synthetic pyrethroid, fenvalerate tofreshwater catfish Clarias gariepinus and the role of dietary supplementation of ascorbic acid to ameliorate the toxic effectsof the pesticide. Bioassays were made using a 3X3 factorial design to test three concentrations of fenvalerate (0, 0.58, and 2.9g.L-1) and three levels of ascorbic acid (0, 50 and 100 mg/100 g diet). Chronic exposures to the sub-lethal concentrations offenvalerate increased mortality and reduced growth of the fish in a dose-dependent way. Ascorbic acid concentrations decreasedin the kidney and increased in the liver of the fish following chronic exposure to fenvalerate. Fish fed a dietary supplementof ascorbic acid showed higher growth and increased capacity to counteract the ill effects of fenvalerate. A supplement of50 mg ascorbic acid per 100 g diet was found adequate to induce higher growth in control fish, while a higher concentrationof ascorbic acid (100 mg/100 g diet) was necessary to counteract the effects of chronic exposure to fenvalerate. However,even the higher ascorbic acid supplement (100 mg/100 g diet) could not protect against the detrimental effects of 2.9 g.L-1fenvalerate.

Key words:Pyrethroid; fenvalerate; fish; toxicity; ascorbic acid.

* Author for correspondence, email: [email protected], akaviraj@gmail

INTRODUCTIONFenvalerate is the most widely used compound of thecyanophenoxy-benzyl group of the synthetic pyrethroidpesticides and is registered for use in agriculture to protecta wide variety of crops including cotton, soybeans, corn,vegetables, apples, peaches, pears and nuts from insect pests(Beyond Pesticides 2000). In India, the pesticide is usedprimarily to control pests of cotton and vegetables (Madanet al. 2000). The pesticide enters aquatic ecosystems throughvarious routes and poses a risk to many non-target aquaticorganisms, particularly those inhabiting water bodies adjacentto agricultural fields. Although synthetic pyrethroids havebeen claimed as safe and environmentally friendly becauseof their selective toxicity to insects, low persistence and lowtoxicity to mammals and birds, they are highly toxic to anumber of other non-target organisms including fish, lobster,

shrimp, mayfly nymphs and many species of zooplankton(Bradbury and Coats 1989; Oudou et al. 2004). Becauseof impending bans on many chlorinated hydrocarbon,organophosphorous and carbamate pesticides there has been adramatic rise in the use of fenvalerate in recent years and thecurrent information is not sufficient to adequately assess therisk posed by fenvalerate to non-target organisms (Sanchez-Fortun and Barahona 2005).

Fenvalerate is relatively stable under field conditions withhalf-lives ranging from 15 days to 3 months in soil, 21 days inwater and 2-4 weeks in vegetation (Beyond Pesticides 2000),and it has the potential to affect the mortality and growth of

fish once it enters aquatic ecosystems. The main objectiveof this study was to evaluate how mortality and growth offreshwater catfish, Clarias gariepinus,which are culturedin swamps and derelict water bodies often contaminated by

agricultural run offs, are affected by chronic exposure to sub-lethal concentrationsof fenvalerate. Another objective of thisstudy was to evaluate if a dietary supplement of ascorbic acid(AA) could reduce the toxicity of fenvalerate to fish. Tripathi(1992) observed that Clarias batrachus, another freshwatercatfish of India that is cultured in swamps and derelict waterbodies, was less sensitive to fenvalarate (LC50: 9.4 g.L-1)as compared to aldrin (LC50:

0.36 g.L-1), an organochlorine

pesticide belonging to the cyclodiene group. In contrast,C. batrachus was more sensitive to fenvalerate than tocaptan (LC50: 547 g.L-1), a thiophthalimide fungicide, orto diazinon (LC50: 2420 g.L-1), an organophosphorouspesticide. Harmful biochemical effects of fenvalerate at sub-lethal concentrations have also been observed on some otherswamp-inhabiting Indian fish like Channa punctatus(Sethand Saxena 2003), and freshwater pond bottom dwellers like

Cirrhinus mrigala(Mushigeri and David 2004). However,information is lacking on how chronic exposure of fenvalerateat sub-lethal concentrations can affect the growth of thefreshwater fish.

Ascorbic acid (AA) is an important intracellular antioxidant

and is involved in the self-defence mechanisms of fish. It

works as an antitoxic agent against heavy metals (Patel

and Rao 1999), pesticides (Guha et al. 1993) and microbial

assaults in fish (Sobhana et al. 2002). A high level of AA also

results in increased tolerance of juvenile fish to intermittent

hypoxic stress (Ishibashi et al. 1992). However, many fish

cannot synthesise AA de novo; these require an exogenous

supply for optimum growth and self-defence (Ai Q et al.2004). Ascorbic acid requirements of fish for natural growth

vary from species to species. Mishra and Mukhopadhyay

(1996) observed the best growth of freshwater catfish


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Clarias batrachus with supplementation of 200 mg

AA/ kg diet (since AA is unstable and its activity is lost during

processing and storage, incorporation of 200 mg AA/kg led

to an actual level of 69 mg AA/kg), while Merchie et al.

(1995) observed a much higher requirement for AA (2000

g AA/g of diet) by Clarias gariepinusfor optimal growth.

We (Datta and Kaviraj, 2003) observed earlier that 50 mg

/100g of AA incorporation (actual level 23.7 mg AA/100

g diet) initiated a high growth in Clarias gariepinus, but a

higher dose (100 mg/100 g; actual level, 43.8 mg AA/100

g diet) was required to overcome the stress of the synthetic

pyrethroid deltamethrin. This level is much higher than the

dose required for better growth of C. batrachus, but still less

than the dose which Merchie et al. (1995) observed to produce

a positive effect on the growth of C. gariepinus. Both 50 and

100 mg AA per 100 g of diet were used in the present study

to evaluate if dietary incorporation of AA could be used as a

possible tool to counteract the toxicity of fenvalerate to the

freshwater catfish Clarias gariepinus.

MATERIALS AND METHODS

Test fishFingerlings (mean length 5.0 0.2 cm, mean weight2.0 0.2 g) of Clarias gariepinuswere procured from a localhatchery and were acclimatised to the test conditions for 120hours before use. During acclimatisation the test fish werefed with a mixture of rice bran and mustard oil cake (1:1)ad libitum.

Test chemical

TATAfen 20 EC (Rallis India Ltd, Mumbai ), with fenvalerate[(RS)cyano-3-phenoxybenzyl (RS) 2-(4-chlorophenyl)-3-methylbutyrate] as the active ingredient, was used as the testchemical. The required amount of the chemical was dissolvedin water to make a 100 mg L -1aqueous stock solution offenvalerate. The necessary dilutions of the stock solutionwere then carried out to prepare the desired concentrationsof fenvalerate for the bioassays.

BioassaysSixty-day static renewal bioassays were conducted outdoorsin 60-liter earthen vats following the recommendations of

APHA (1995). The test medium was water drawn from a300-meter-deep tube-well and stored in an overhead tank.The physicochemical properties of the water were: pH, 9.1 0.1; free CO2, 4.0 0.5; DO, 7.2 0.5; alkalinity 60 4;and hardness 201 12 mg/L. Each vat was provided with3 cm-thick soil sediment at the bottom and was kept filledwith water for about one month before the bioassay wasstarted. Such conditioning of earthen vats allows minimumpercolation of water. Growth of the plankton population in thevat water was checked every week. Random samples of waterwere collected from the vats by plankton net, concentratedby filtration through the plankton net and plankton densitieswere determined microscopically. When sufficient planktongrew to serve as natural food for the experimental fish, eachvat was stocked with 15 acclimatised fingerlings of Clariasgariepinus, followed by treatment of fenvalerate. Altogether27 such conditioned vats were used in a 3 x 3 factorial

design so that three nominal concentrations of fenvaleratecould be tested for each of the three levels of dietary AAsupplement, thereby making nine treatment groups each withthree replicates (Table 1). Three nominal concentrations offenvalerate were used, 0 (F0), 0.58 (F1) and 2.9 (F2) g.L-1.

Every 10 days, 10% of the test medium was renewed with apulsed treatment of fenvalerate at 10% of the initial nominalconcentration.

To provide the dietary supplement of the AA, a basal dietwith 30% crude protein was prepared using rice bran, mustardoilcake and fish meal (see Datta and Kaviraj 2003). The basaldiet itself served as the level 0 of the dietary supplement of AA(A0), and it was fortified with two other levels of AA (50 and100 mg AA per 100 g basal diet) to make dietary supplementlevels 1 and 2 of AA (A1 and A2), respectively. Vitamin Ctablets (Celin Glaxo, India) were used as the source of AA.Since AA is sensitive to heat and moisture and its potency is

lost over long storage, only a weeks ration was prepared atany one time to minimize storage loss of ascorbic acid. Thestorage loss for the two levels of AA (50 and 100 mg / 100 gdiet) was found to be 52.6% and 56.2% respectively (Dattaand Kaviraj 2003). The fish were provided with a ration at10% of the body weight of the fish stocked for six days aweek. Every 15 days the fish were sampled and weighed toadjust the ration.

Sampling and analytical methodsSamples of water were collected from each vat every 10 daysto determine the pH, hardness, alkalinity, dissolved oxygen,free CO

2and temperature of the water. Standard methods

(APHA 1995) were followed for these determinations.Mortality of the fish, if any, was examined daily. Fish weresampled at the end of the bioassay. Length and weight of thesampled fish were taken to determine weight gain (%), foodconversion ratio (FCR), and specific growth rate (SGR).The whole liver was removed from each fish and weighedto calculate the hepato-somatic index (HSI). The ascorbicacid level in the liver and kidney of the sampled fish wasdetermined by the method of Nino and Prasad (1980).

Statistical analysesData from all dependent variables were analysed by

MANOVA and test statistics using Wilksand Roys LargestRoot. Since a significant interaction was found betweenfenvalerate and AA, contrast between levels of pesticidefor each level of AA was tested by contrast analysis forMANOVA (Johnson and Wichern 2005).

RESULTSThe values of hepato-somatic index (HSI), percent increasein weight, food conversion ratio (FCR), specific growth rate(SGR) and average mortality (%) of Clarias gariepinusaregiven in Table 2. Treatment with fenvalerate (T4 and T7)significantly reduced growth of the fish as compared to thecontrols (T1). Dietary supplement of AA influenced thegrowth of both the control and treated fish. The higher levelof fenvalerate (T7; 2.9 g.L-1), produced huge mortality ofthe experimental fish (63%, Table 1). Dietary supplement ofAA reduced the mortality level significantly. Ascorbic acid


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Table 1.Mortality (%), hepatosomatic index (HSI) and growth of C. gariepinus after 60 days of exposure to different treatments. Valuesare mean of three replicates SD

Table 2.Results of MANOVA run in 3 X 3 full factorial design (without intercept) to test significance of difference between levels offenvalerate, ascorbic acid and interaction between fenvalerate and ascorbic acid.

levels in liver showed an increase with the increase in thelevel of fenvalerate, while kidney AA level decreased withthe increase in the level of fenvalerate (Figure 1).

Results of MANOVA (3 X 3 full factorial design withoutintercept) showed that the effects of fenvalerate, AA and theinteraction between fenvalerate and AA were significant atthe 1% level (Table 2). The contrast analyses showed that

for ascorbic acid level 0 (no AA) and 1 (50 mg AA / 100 gdiet) the three levels of fenvalerate (0, 0.58 and 2.9 g.L-1)produced significantly different effects from each other forall the parameters except HSI at 1% level. For AA level 2(100 mg AA / 100 g diet) the effects between the two levels offenvalerate (0 and 0.58 g.L-1, T3 and T6) were not significantfor any of the parameters except kidney AA, which showed asignificant difference between these two levels of fenvalerate,at the 1% level. However, even for AA level 2 the effect of2.9 g.L-1 fenvalerate was significantly different from both0 and 0.58 g.L-1fenvalerate (T6) at both the 1% and 5%levels. Temperature and dissolved oxygen in the test waters

ranged between 30-33C and 7.2 - 9.3 mg.L-1

, respectively,during the bioassay. Other water quality parameters were alsowithin the normal range and there was no significant variationbetween the treatments.

DISCUSSIONSixty-day chronic exposure to the highest sub-lethalconcentration of fenvalerate tested in the present investigation,(2.9 g L-1; T7; F2A0), reduced the growth of C. gariepinusto less than 50% and doubled the FCR as compared to thecontrol (T1; F0A0). The lower sub-lethal concentration (0.58g l-1; T4; F1A0) of the pesticide tested was less toxic, but

still reduced the growth significantly as compared to control.These effects of fenvalerate resemble those reported bySheela et al. (1992), who observed that exposure of Channastriatusto 0.4 to1.0 g L-1fenvalerate decreased the rate offeeding, absorption, growth and conversion efficiency ofthe fish.Due to its lipophilicity, fenvalerate is absorbed at ahigh rate through the gills of fish. However fish have a poorability to metabolise and excrete fenvalerate (Bradbury et al1985) and thus are susceptible to even minute concentrationof the pesticide. A reduction of structural and solubleproteins in liver, brain and muscle was found in Cyprinuscarpio following exposure to 10 g/L of fenvalerate for 6to 48 h (Reddy et al. 1991). Chronic exposure can bring outthese effects in fish even at much lower concentration offenvalerate. In addition, the aquatic invertebrate communityis very sensitive to fenvalerate.Woin (1998) observed thatexposure of freshwater ponds to 0.54 - 1.3 g L-1 fenvalerate

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resulted in structural changes in the macrobenthic communityof the pond, which persisted for long periods. Daphnidsalso suffered a huge mortality and reduction in long termgrowth following a 24-h pulse exposure to six levels ofsub-lethal concentrations (0.03 to 3.2 g L-1) of fenvaleratein a laboratory mesocosm study (Pieters et al. 2005). These

studies indicate that growth of fish food organisms is likelyto be hampered at concentrations of fenvalerate tested inthe present study, thereby putting a pressure on the growthof the fish.

The present investigation revealed more than 60% mortalityof C. gariepinus after 60 days exposure to 2.9 g L-1fenvalerate. Tripathi (1992) observed 50% mortality ofClarias batrachus after 40 days exposure to 9.4 g L-1fenvalerate. A dietary supplement of AA (Ascorbic acid,vitamin C) at 100 mg/100 g basal diet significantly reducedmortalities in the control as well as the treated fish. Clariasgariepinus, if deprived of AA in the diet, develops anaemia

and becomes susceptible to pathogenic agents (Adham et al.2000). Dietary supplementation of AA has also been found toincrease the survival and resistance to environmental stress ofthe larvae of the shell-fish spiny lobster (Smith et al. 2004).

Figure 1.Changes in ascorbic acid (AA) level in liver and kidneyof the experimental fish after 60 days exposure to three levels offenvalerate under different dietary AA levels.

In addition to reduction in mortality rate, dietarysupplementation of AA increased the AA level in the liverof C. gariepinus, increased growth of the fish in the controltreatments and prevented reduction of growth of the fishinduced by fenvalerate. A strong correlation between the

growth and tissue AA levels in fish has been observed bymany workers (Mishra and Mukhopadhyay 1996; Xiaojie etal. 2003; Lin and Shiau 2005). Most teleost fish are unableto synthesize AA due to lack of L-gulonolactone oxidase,the enzyme responsible for the synthesis of ascorbic acid,and thus require an exogenous source of AA in the diet (AiQ et al. 2004). Mishra and Mukhopadhyay (1996) observedthe best growth of freshwater catfish Clarias batrachuswithsupplementation of 200 mg AA/kg diet (actual level 69 mg/kg). We observed the best growth of Clarias gariepinus whenthe diet was supplemented with 50 mg AA/100 g diet (actuallevel 23.7 mg AA/100 g diet) i.e. 500 mg AA/kg diet (actuallevel 237 mg/kg diet). The results of the present study showed

that fish fed with a low level of AA (50 mg /100 g diet) wereunable to counter the stress produced by fenvalerate, whilefish fed with a high level of AA (100 mg/100 g diet) couldcounter the stress of 0.58 g.L-1 fenvalerate, but failed tocounter the stress of 2.9 g.L-1 of fenvalerate. The levelof AA supplementation which is capable of counteractinga stress, depends on the type of stress. It has beendemonstrated that doses up to 8 or 10 times the normal dietaryrequirements are necessary to achieve increased wound repair,resistance against infections or reproductive success (Li andLovell 1985).

Chronic exposure to fenvalerate induced an increase in liver

AA level, but a decrease in kidney AA level. In a mammaliansystem (rat) the plasma AA level increases rapidly due tostress (Ognjanovi et al. 2003). Ascorbic acid is involvedin intermediary metabolism. Its dietary inclusion increasesthe activity of various enzymes like hexokinase, pyruvatekinase, glycerol kinase, glucose 6 PO

4dehydrogenase (G6

PDH), malic enzyme (ME), glutamate pyruvate transaminase(GPT) in fish (Prez et al. 2006). Liver being the principalsite of such metabolism, AA is transported to the liverfrom kidney and other tissues through circulation therebydecreasing the AA level in these tissues and increasing theplasma level of AA during the transport. Therefore, increase

in the level of AA in the plasma or liver is an indication thatit is involved in the mechanism of detoxification of toxicantsand counteraction of the stress. Ascorbic acid also plays animportant role in the regeneration of reduced form of VitaminE (Tanaka et al. 1997), which is a liposoluble antioxidant andhelps in stabilising the cell membranes, thus maintaining theirpermeability (Navarro et al. 1999). Ascorbic acid is thus ableto prevent indirectly the pyrethroid induced interference ofsodium ion permeability in stimulated nerve membranes(Shafer and Meyer 2004).

In natural water, algae seem to be an important source ofAA for aquatic animals (Olsen et al. 2000). However, this

source is inadequate to counter the acute stress producedon fish by pyrethroid pesticides. Therefore, an additionaldietary supply of AA is required for the fish exposed tothese pesticides. It is concluded from the present study that


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fenvalerate is capable of producing chronic toxicity to fisheven at a low dose (0.58 g L -1) and in situations like thisnormal dietary requirement of AA in the diet of fish shouldbe at least doubled to overcome the predictable ill effects ofthe pesticide on growth of the fish.

ACKNOWLEDGEMENTWe thank the Head, Department of Zoology, University ofKalyani, for providing necessary facilities for this research.

REFERENCESAi Q, Mai K, Zhang C, Xu W, Duan Q, Tan B and Liufu Z.2004. Effects of dietary vitamin C on growth and immuneresponse of Japanese seabass, Lateolabrax japonicus.

Aquaculture242, 489-500.

Adham KG, Hashem HO, Abu-Shabana MB and Kamel AH.2000. Vitamin C deficiency in the catfish Clarias gariepinus.

Aquaculture Nutrition6,129-139.APHA. 1995. Standard Methods for the Examination ofWater and Wastewater.American Public Health Association,American Water Works Association and Water PollutionControl Federation,Washington, DC, U.S.A.

Beyond Pesticides. 2000. Synthetic PyrethroidsChemicalWATCH Factsheet. Pesticides and You 20 (3):12-14. http://www.beyondpesticides.org/pesticides/factsheets/Synthetic%20Pyrethroids.pdf [accessed 25th Sept. 2006].

Bradbury SP and Coats JR. 1989. Toxicokinetics andtoxicodynamics of pyrethroid insecticides in fish.

Environmental Toxicology and Chemistry8, 373-380.Bradbury SP, Coats JR and McKim JM. 1985. Differentialtoxicity and uptake of two fenvalerate formulations in fatheadminnows (Pimephales promelas).Environmental Toxicologyand Chemistry4,533-541.

Datta M and Kaviraj A. 2003. Ascorbic acid supplementationof diet for reduction of deltamethrin induced stress infreshwater catfish Clarias gariepinus. Chemosphere 53,883-888.

Guha D, Dutta K and Das M. 1993. Vitamin C as antitoxicfactor in DDT induced haematotoxicity in Clarius batrachus.

Proceedings of the Zoological Society(Calcutta) 46,11-15.Ishibashi Y, Kato K, Ikeda S, Murata O, Nasu T and KumariH. 1992. Effect of dietary ascorbic acid on tolerance tointermittent hypoxic stress in Japanese parrot fish. NipponSuisan Gakkaishi58, 2147-2152.

Johnson RA and Wichern DW. 2005.Applied MultivariateStatistical Analysis. Pearson Education of India, Delhi, India,pp 307-309.

Li Y and Lovell RT. 1985. Elevated levels of dietary ascorbicacid increase immune responses in channel catfish.Journalof Nutrition115,123-131.

Lin MF and Shiau SY. 2005. Dietary L-ascorbic acid affectsgrowth, nonspecific immune responses and disease resistancein juvenile grouper,Epinephelus malabaricus. Aquaculture244,215-221.

Madan VK, Singh R, Kumari B, Naresh JS and KathpalTS. 2000.Dissipation of lindane and fenvalerate residuesin chickpea (Cicer arietinumL.) under Indian climaticconditions. Ecotoxicology and Environmental Safety 46,163-166.

Merchie G, Lavens P, Dhert PH, Pector R, Mai SAF, Abbes M,Nelis H, Ollevier F, De Leenhee A and Sorgeloos P. 1995. Livefood mediated vitamin C transfer to Dicentrarchus labraxand Clarius gariepinus.Journal of Applied Ichthyology11,336-341.

Mishra S and Mukhopadhyay PK. 1996. Ascorbic acidrequirement of catfish fry Clarias batrachus(Linn.).Indian

Journal of Fisheries43, 157-162.

Mushigeri SB and David M. 2004. Accumulation offenvalerate and related changes in lactate and succinatedehydrogenases activity in functionally different tissues of

the freshwater fish, Cirrhinus mrigala(Hamilton).Journalof Basic and Clinical Physiology and Pharmacology 15,143-52.

Navarro F, Arroyo A, Martin SF, Bello RI, de Cabo R,Burgess JR, Navas P and Villalba JM. 1999. Protective roleof ubiquinone in vitamin E and selenium-deficient plasmamembranes.BioFactors9,163-170.

Nio HV and Prasad AS. 1980. Ascorbic acid, (vitaminC). In Vitamins and Trace Elements - Gradwohls Clinical

Laboratory Methods and Diagnosis. Volume I. SonnenwirthAC and Jarett L. (Eds), The C.V. Mosby Co. London, UK,pp 370-372.

Ognjanovi BI, Pavlovi SZ, Maleti SD, iki RV, tajn A,Radojii RM, Saii ZS and Petrovi VM. 2003. Protectiveinfluence of vitamin E on antioxidant defense system in theblood of rats treated with cadmium. Physiological Research52,563-570.

Olsen AI, Mland A, Waagb R and Olsen Y. 2000. Effectof algal addition on stability of fatty acids and some water-soluble vitamins in juvenileArtemia franciscana. Aquaculture

Nutrition6,263-273.

Oudou HC, Alonso RM and Bruun Hansen HC. 2004.Voltammetric behaviour of the synthetic pyrethroid lambda-

cyhalothrin and its determination in soil and well water.Analytica Chimica Acta523, 69-74.

Patel G and Rao MV. 1999. Role of ascorbic acid on mercuricchloride toxicity in vital organs of mice. Indian Journal of

Environmental Toxicology9, 53-55.

Prez JA, Hidalgo MC, Morales AE, Abelln E, Arizcun Mand Cardenete G. 2006. In proceedings, Effects of dietaryVitamin C on intermediary metabolism in Dentex dentex(Abstract). XIIthInternational Symposium on Fish Nutritionand Feeding, Biarritz, France, May 28- June 1, 2006, p190.

Pieters BJ, Paschke A, Reynaldi S, Kraak MH, AdmiraalW and Liess M. 2005. Influence of food limitation on theeffects of fenvalerate pulse exposure on the life history andpopulation growth rate of Daphnia magna. EnvironmentalToxicology and Chemistry24,2254-2259.

Vol. 12, pp. 129-134, 2006



6/6

134


Reddy PM, Philip GH and Bashamohideen M. 1991.Fenvalerate induced biochemical changes in the selectedtissues of freshwater fish, Cyprinus carpio.Biochemistry

International 23,1087-96.

Sanchez-Fortun S and Barahona MV. 2005. Comparative

study on the environmental risk induced by severalpyrethroids in estuarine and freshwater invertebrateorganisms. Chemosphere59, 553-559.

Seth N and Saxena KK. 2003. Hematological responsesin a freshwater fish Channa punctatus due to fenvalerate.

Bulletin of Environmental Contamination and Toxicology

71, 11921199.

Shafer TJ and Meyer DA. 2004. Effects of pyrethroids onvoltage-sensitive calcium channels: a critical evaluationof strengths, weaknesses, data needs, and relationship toassessment of cumulative neurotoxicity. Toxicology and

Applied Pharmacology196,303-318.Sheela M, Mathivanan R, Muniandy S. 1992. Impact offenvalerate and phosphamidon on food intake, growth andconversion efficiency in the fish Channa striatus (Bloch).

Environment and Ecology10, 593-596.

Smith GG, Brown MR and Ritar AJ. 2004. Feeding juvenileArtemiaenriched with ascorbic acid improves larval survival

in the spiny lobsterJasus edwardsii.Aquaculture Nutrition10,105-112.

Sobhana KS, Mohan CV and Shankar KM. 2002. Effectof dietary Vitamin C on the disease susceptibility andinflammatory response of mrigal, Cirrhinus mrigala

(Hamilton) to experimental infection of Aeromonashydrophila.Aquaculture207, 37-48.

Tanaka K, Hashimoto T, Tokumara S, Iguchi H and KojoS. 1997. Interactions between vitamin C and vitamin E areobserved in tissues of inherently scorbutic rats. Journal of

Nutrition127,2060-2064.

Tripathi G. 1992. Relative toxicity of aldrin, fenvalerate,captan and diazinon to the freshwater food fish Clariusbatrachus.Biomedical and Environmental Sciences 1,33-38.

Woin P. 1998. Short- and long-term effects of the pyrethroidinsecticide fenvalerate on an invertebrate pond community.

Ecotoxicology and Environmental Safety41, 137-146.Xiaojie Wang, Kang-Woong Kim, Sungchul C Bai, Min-DoHuh and Byong-Youl Cho. 2003. Effects of the differentlevels of dietary vitamin C on growth and tissue ascorbic acidchanges in parrot fish (Oplegnathus fasciatus).Aquaculture215, 203-211.


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