OA 학술지
Synergistic Effects of Dietary Vitamins C and E on Methylmercury-Induced Toxicity in Juvenile Olive Flounder Paralichthys olivaceus
  • cc icon
  • cc icon

This experiment was conducted to evaluate the synergistic effects of vitamin C and E on methylmercury (MeHg) toxicity in juvenile olive flounder Paralichthys olivaceus. In a 3×3 factorial design, 9 experimental diets containing three different vitamin C (0, 200 or 400 mg/kg diet in the form of l-ascorbyl-2-monophosphate) and vitamin E (0, 100 or 200 mg/kg diet in the form of dl-α-tocopheryl acetate) levels with the Hg toxicity level (20 mg/kg diet in the form of MeHg) were formulated. Triplicate groups of fish averaging 2.3 ± 0.05 g (mean ± SD) were fed one of the 9 diets in a flow through system for 8 weeks. Fish fed 400 mg vitamin C/kg diet with 100 or 200 mg vitamin E/kg diet showed significantly (P < 0.05) higher weight gain (WG) than did fish fed the other diets. Fish fed 400 mg vitamin C/kg diet at all vitamin E levels and those which fed vitamin C and E equally at a rate of 200 mg/kg diet showed significantly (P < 0.05) higher feed efficiency (FE), specific growth rate (SGR) and protein efficiency ratio (PER) than did fish fed the other diets. Fish fed 200 and 400 mg vitamin C/kg diet exhibited significantly (P < 0.05) lower Hg concentration in their muscle as well as kidney than did fish fed the other diets. Therefore, these results clearly indicated that the synergistic effects of these two vitamins on MeHg toxicity by supplementing dietary vitamin C (200 and 400 mg/kg diet) with vitamin E (100 and 200 mg/kg diet) in juvenile olive flounder.

Paralichthys olivaceus , Methylmercury , Bioaccumulation , Vitamin C , Vitamin E
  • Introduction

    Mercury (Hg) is a naturally occurring element found in air, water, and soil. It exists in the environment in three oxidation states Hg (0), Hg (I), and Hg (II). Microbial methylation in aquatic ecosystems is a crucial component of the Hg cycle in the environment (Wiener et al., 2003). Once in surface water, Hg enters a complex cycle whereby one form can be converted to another. Mercury attached to particles can settle onto sediments where it can diffuse into the water column, be resuspended, and be buried by other sediments, or be methylated. Methylmercury (MeHg) can enter the food chain, or it can be released back to the atmosphere by volatilization (During et al., 2009).

    Fish naturally absorb MeHg into their tissues directly from water as it passes over their gills and by eating other contaminated foods, including fish (Roe, 2003). Mercury contamination in commercial fish feeds also occurs due to high metal levels in the raw materials (Wang et al., 2012). For this reason, dietary exposure is one of the routes of Hg contamination in fish (Choi and Cech, 1998). As a result, Hg has been regarded as undesirable substance in animal feed (EFSA, 2008).

    Seafood contamination by MeHg is a public health concern, particularly in countries with high rates of fish consumption, such as Korea. In line with this, olive flounder is among marine fishes being preferred by consumers in Korea. Daily seafood consumption has reached 50.6 g, which accounts for ~3.8% of the total food ingested (Moon et al., 2009; Choi et al., 2012). Consequently, high blood Hg levels in a representative sample of the Korean adult population were associated with fish consumption (Kim and Lee, 2010). Accordingly, Moon et al. (2011) suggested implementation of systematic monitoring programs for seafood contamination by Hg in Korea. Limiting fish consumption was also suggested as a mechanism to avoid MeHg intake (Dorea and Barbosa, 2005).

    Methylmercury is a neurotoxicant that affects the developing nervous system of humans and has been linked to neurological problems (Davidson et al., 2010). The various toxic effects induced by Hg in biological systems are due to alterations in the antioxidant defense system (Sheweita, 1998; Berntssen et al., 2003; Alves et al., 2007; Berg et al., 2010). Moreover, MeHg has been shown to cause coronary heart disease in humans (Wang et al., 2012) and decreased levels of nutrients in rats (Fukino et al., 1984).

    Antioxidants such as vitamin C, vitamin E, and selenium (Se) decrease Hg toxicity in Japanese quail (Kung et al., 1987) and various other organisms (Chapman and Chan, 2000; Agarwal et al., 2010; Al-Attar, 2011). Bapu et al. (1994) examined the effects of vitamin C treatment after subcutaneous injections of methylmercuric chloride (MeHgCl) for 7 days in mice and found improved recovery of enzymatic activities.

    Extensive work has emphasized the damage caused by heavy metal toxicity, but the combined ameliorative effect of vitamin C and E on MeHg contamination in fish should be investigated. Thus, the objective of this study was to evaluate the combined effects of vitamin C and E on tissue Hg, as well as growth-related problems, in juvenile olive flounder as the result of MeHg.

    Materials and Methods

      >  Experimental diets

    Nine diets with three vitamin C levels (0, 200 and 400 mg/kg diet in the form of l-ascorbyl-2-monophosphate) and three vitamin E levels (0, 100 and 200 mg/kg diet in the form of dl-α-tocopheryl acetate) with Hg (20 mg/kg Hg diet in the form of MeHg) were formulated (Tables 1 and 2). The 20 mg/kg MeHg diet was chosen based on a previous study (unpublished) that was conducted for 5 weeks in our laboratory and showed relatively lower mortality. In diets supplemented with MeHg and ascorbic acid sources, an equivalent amount of cellulose was removed. In a 3 × 3 factorial design these nine experimental diets (C0E0, C0E100, C0E200, C200E0, C200E100, C200E200, C400E0, C400E100 and C400E200) were formulated to be isonitrogenous and isoenergetic, containing 50% crude protein (CP) and 16.7 kJ available energy/g diet. The energy levels of diets were calculated based on 16.7, 16.7, and 37.7 kJ g-1 for protein, carbohydrate, and lipid, respectively (NRC, 2011). Vitamin-free casein was used as the main protein source. All the ingredients were mixed completely and then pelleted using 1- and 2-mm diameter dies (Bai and Lee, 1998). After processing, all diets were packed into small bags and stored at -20℃ until use.

      >  Experimental fish and feeding trials

    Juvenile olive flounder were obtained from Tong-Yeong, Korea. Prior to the start of the feeding trial, fish were fed the basal diet for 10 days as an adjustment to the semi-purified diet, and to deplete vitamin C reserves. The feeding trial was performed in a flow through system with 30 L aquaria receiving filtered seawater at a rate of 2 L/min. Supplemental aeration was provided to maintain dissolved oxygen near saturation. Water temperature was kept at 20 ± 1℃. Twenty experimental fish with a mean weight of 2.3 ± 0.05 g (mean ± SD) were randomly distributed into each aquarium. Each diet was fed to triplicate groups to satiation level three times per day at a feeding rate of 2.0 to 3.5% of wet body weight. Total fish weight in each aquarium was determined every 3 weeks, and the amount of diet fed to the fish was adjusted accordingly.

      >  Growth performance

    Growth performance was evaluated using weight gain (WG), specific growth rate (SGR), feed efficiency (FE), and the protein efficiency ratio (PER).

    WG was calculated using the following formula:


    SGR was calculated using the following formula:


    FE and the PER were calculated using the following formulas:


      >  Sample collection and analysis

    After the final weighing, three fish were randomly removed from each aquarium and sacrificed with a lethal dose of benzocaine anesthetic (CAS, Canada). Proximate composition analyses of experimental diets were performed using standard methods (AOAC, 1995). Samples of diets were dried to a constant weight at 105℃ to determine moisture content. Ash content was determined by incineration at 550℃, crude lipid content was determined by Soxhlet extraction using the SOXTEC SYSTEM 1046 (FOSS, Hoganas, Sweden), and crude protein content was determined by the Kjeldahl method (N × 6.25), after acid digestion.

      >  Vitamin C and E analysis

    Ascorbic acid and α-tocopherol concentrations of the diet and tissue were determined by high performance liquid chromatography (HPLC; DIONEX, SOFTRON, USA). For ascorbic acid, the ultraviolet detector was set to 254 nm. The mobile phases for ascorbic acid and α-tocopherol were 0.05 M KH2PO4 and hexane: isopropanol (98:2, v/v), respectively. The flow rate for both was 1.0 mL/min. Weighed samples were homogenized in 10% cold metaphosphoric acid (for ascorbic acid) and in 5-mL ethanol (for α-tocopherol). Homogenates were centrifuged at 3,000 g for 20 min and supernatants were analyzed after filtration through a 0.45-μm pore-size syringe filter.

      >  Mercury analysis

    Greater than 90% of Hg present in fish is in the form of MeHg. Therefore, the total concentration of Hg was measured instead of MeHg (Bloom, 1992; Amlund et al., 2007). A direct Hg analyzer (DMA-80, Milestone, Inc., Shelton, CT) was used to determine the tissue Hg concentration; the method followed that of Lee et al. (2011). A certified reference material (DORM-2 dogfish liver, National Research Council, Canada) was used simultaneously during the analyses.

      >  Statistical analysis

    Data were analyzed by two-way ANOVA to test the effect of the dietary treatments. Least significant difference (LSD) was used to compare means when a significant treatment effect was identified. SPSS version 16.0 (SPSS Inc., Chicago, IL, USA) was used and P-values of ≤ 0.05 were considered to indicate statistical significance.


      >  Growth performance

    After 8 weeks of feeding, fish that were fed 400 mg/kg vitamin C at all vitamin E levels had better growth performance, compared to the other groups. Significantly higher (P < 0.05) WG was exhibited by the C400E200 and C400E100 feeding groups. In general, WG appeared to decrease with decreasing amounts of vitamin C. Consequently, fish that were fed MeHg-containing diets without vitamin C and E showed significantly lower WG than the other groups. Other growth performance parameters such as FE, SGR and PER were found to be significantly higher (P < 0.05) for fish fed diets containing 400 mg/kg vitamin C at all vitamin E levels, and for those that were on the C200E200 diet (Table 3).

      >  Tissue Hg burden

    Muscle Hg concentrations in fish that were fed diets comprising 200 and 400 mg/kg vitamin C were significantly lower (P < 0.05) than other feeding categories at all vitamin E levels, with the exception of the C200E0 group. In other words, significantly higher muscle Hg accumulation was observed in fish on the C0E100, C0E200 and C200E0 diets. Significantly lower (P < 0.05) Hg concentrations in the liver were observed in fish fed diets supplemented with 400 mg/kg vitamin C and 200 mg/kg vitamin E. The remaining diets containing 400 mg/kg vitamin C also resulted in a significant reduction in liver Hg (P < 0.05) compared to those that received 0 and 200 mg/kg vitamin C. Fish fed diets with 0 mg/kg vitamin C and 100 and 200 mg/kg vitamin E accumulated significantly more (P < 0.05) Hg in their liver than fish in the other groups, with the exception of the C200E0 feeding group. Nevertheless, no significant difference (P < 0.05) in kidney Hg concentration was detected between fish fed 200 and 400 mg/kg vitamin C and 100 and 200 mg/kg vitamin E. On the other hand, those fish that were on diets without vitamin C (C0E100 and C0E200) accumulated significantly more (P < 0.05) Hg in the kidney (Table 4).


    Although the effects of Hg on fish are complex and multiple (Weis, 2009), MeHg is known to cause oxidative stress, causing damage to vital components of the biological system, from mitochondrial damage to altered behavior (Berntssen et al., 2003; Alves et al., 2007; Berg et al., 2010). The high affinity of methylmercury for the thiol or sulfhydryl (-SH) groups of proteins underlies its mechanisms of toxicity (NRC, 2005). Therefore, the poor growth performance observed in olive flounder fed diets that did not contain vitamin C and/or E (C0E0, C0E100, C0E200, C200E0 and C400E0) might have occurred due to decreased enzyme activity, altered structural functionality, or transport process problems caused by Hg accumulation (Zalups and Lash, 1994). All such functional disturbances might have been caused by excessive release of reactive oxygen species (ROS) driven by Hg accumulation (Bansal et al., 1992; Lund et al., 1993). Consistent with the findings in this study, impaired growth and poor gonad development caused by dietary MeHg have been reported in juvenile walleye (Friedmann et al., 1996), Sacramento blackfish (Houck and Cech Jr, 2004) and Green & White sturgeon (Lee et al., 2011).

    Excessive release of ROS and increased lipid peroxidation in cells are harmful effects that occur during Hg accumulation (Bansal et al., 1992; Lund et al., 1993). Free radicals and the products of peroxidation damage the integrity and function of biomembranes. Vitamin C and E inhibit free radical formation and lipid peroxidation (Sies et al., 1992; Aldana et al., 2001; Rao and Sharma, 2001; Kalender et al., 2004; Valko et al., 2005; Agarwal et al., 2010). Low Hg concentrations were observed in muscle and liver of fish that were fed the C400E200 and C400E100, and C400E200 diets, respectively. This was presumably due to the ability of the antioxidant vitamins to neutralize mercury ions, or bind with transition metals and prevent ROS-mediated oxidative damage in tissues (Ganther, 1980; Nandini and Lata, 2010).

    In the present study, vitamins C and E acted synergistically against Hg accumulation, possibly because of the tendency of vitamin E to maintain vitamin C levels in damaged tissues by inhibiting free radical formation (Duval and Poelman, 1995). Vitamin C is also known to regenerate vitamin E from its oxidized form (Bruno et al., 2006). Therefore, effective dispersal of Hg from –SH groups by these vitamins, along with their ability to inhibit and remove free radicals, might have reduced tissue Hg concentrations and helped to improve growth performance (Fukino et al., 1984; Patil and Rao, 1999; Durak et al., 2010). In agreement with our findings, Guillot et al. (1998) reported that administration of 1,000 mg/kg ascorbic acid reduced Hg accumulation in multiple rat tissues. Rambeck et al. (1996) also confirmed the role of ascorbic acid to reduce the retention of inhaled Hg vapor. Durak et al. (2010) strengthened the present study`s findings by showing amelioration of Hg-induced toxicity through the combined effects of vitamin C and E, in vitro, using human erythrocytes. The reduction of Hg-driven mortality in Japanese quail (Welsh and Soares, 1976) and improved growth and survival in Hg-exposed rats (Welsh, 1979) as a result of vitamin E supplementation has also been reported. Beyrouty and Chan (2006) also showed that mortality and poor growth resulting from MeHg accumulation in rats could be improved by the synergistic action of vitamin E and Se.

    In conclusion, poor growth performance resulting from MeHg accumulation were alleviated and the Hg concentration in muscle, liver, and kidney were reduced by dietary supplementation of vitamins C (200 and 400 mg/kg) and E (100 and 200 mg/kg) in juvenile olive flounder.

  • 1. Agarwal R, Goel SK, Chandra R, Behari JR 2010 Role of vitamin E in preventing acute mercury toxicity in rat [Environ Toxicol Pharmacol] Vol.29 P.70-78 google doi
  • 2. Al-Attar AM 2011 Vitamin E attenuates liver injury induced by exposure to lead, mercury, cadmium and copper in albino mice [Saudi J Biol Sci] Vol.18 P.395-401 google doi
  • 3. Aldana L, Tsutsumi V, Craigmill A, Silveira MI, Gonzalez de Mejia E 2001 α-Tocopherol modulates liver toxicity of the pyrethroid cypermethrin [Toxicol Lett] Vol.125 P.107-116 google doi
  • 4. Alves RRN, Rosa IL, Santana GG 2007 The role of animal-derived remedies as complementary medicine in brazil [Bioscience] Vol.57 P.949-955 google doi
  • 5. Amlund H, Lundebye A-K, Berntssen MHG 2007 Accumulation and elimination of methylmercury in Atlantic cod (Gadus morhua L.) following dietary exposure [Aquat Toxicol] Vol.83 P.323-330 google doi
  • 6. 1995 Official Methods of Analysis of the Association of Official Analytical Chemists google
  • 7. Bai SC, Lee K-J 1998 Different levels of dietary dl-α-tocopheryl acetate affect the vitamin E status of juvenile Korean rockfish, Sebastes schlegeli [Aquaculture] Vol.161 P.405-414 google doi
  • 8. Bansal AK, Bhatnagar D, Bhardwaj R 1992 Lipid peroxidation and activities of antioxygenic enzymes in vitro in mercuric chloride treated human erythrocytes [Bull Environ Contam Toxicol] Vol.48 P.89-94 google
  • 9. Bapu C, Vijayalakshmi K, Sood PP 1994 Comparison of monothiols and vitamin therapy administered alone or in combinations during methylmercury poisoning [Bull Environ Contam Toxicol] Vol.52 P.182-189 google
  • 10. Berg K, Puntervoll P, Valdersnes S, Goksøyr A 2010 Responses in the brain proteome of Atlantic cod (Gadus morhua) exposed to methylmercury [Aquat Toxicol] Vol.100 P.51-65 google doi
  • 11. Berntssen MHG, Waagbø R, Toften H, Lundebye AK 2003 Effects of dietary cadmium on calcium homeostasis, Ca mobilization and bone deformities in Atlantic salmon (Salmo salar L.) parr [Aquac Nutr] Vol.9 P.175-183 google doi
  • 12. Beyrouty P, Chan HM 2006 Co-consumption of selenium and vitamin E altered the reproductive and developmental toxicity of methylmercury in rats [Neurotoxicol Teratol] Vol.28 P.49-58 google doi
  • 13. Bloom NS 1992 On the chemical form of mercury in edible fish and marine invertebrate tissue [Can J Fish Aquat Sci] Vol.49 P.1010-1017 google doi
  • 14. Bruno RS, Leonard SW, Atkinson J, Montine TJ, Ramakrishnan R, Bray TM, Traber MG 2006 Faster plasma vitamin E disappearance in smokers is normalized by vitamin C supplementation [Free Radic Biol Med] Vol.40 P.689-697 google doi
  • 15. Chapman L, Chan HM 2000 The influence of nutrition on methylmercury intoxication [Environ Health Perspect] Vol.108 P.29-56 google doi
  • 16. Choi M, Moon HB, Choi HG 2012 Intake and potential health risk of butyltin compounds from seafood consumption in Korea [Arch Environ Contam Toxicol] Vol.62 P.333-340 google doi
  • 17. Choi MH, Cech JJ 1998 Unexpectedly high mercury level in pelleted commercial fish feed [Environ Toxicol Chem] Vol.17 P.1979-1981 google doi
  • 18. Davidson PW, Leste A, Benstrong E, Burns CM, Valentin J, Sloane-Reeves J, Huang L-S, Miller WA, Gunzler D, van Wijngaarden E, Watson GE, Zareba G, Shamlaye CF, Myers GJ 2010 Fish consumption, mercury exposure, and their associations with scholastic achievement in the Seychelles child development study [Neurotoxicology] Vol.31 P.439-447 google doi
  • 19. Dorea JG, Barbosa AC 2005 Fish consumption and blood mercury: proven health benefits or probable neurotoxic risk? [Regul Toxicol Pharmacol] Vol.42 P.249-250 google doi
  • 20. Durak D, Kalender S, Uzun FG, Demir F, Kalender Y 2010 Mercury chloride-induced oxidative stress in human erythrocytes and the effect of vitamins C and E in vitro [Afr J Biotechnol] Vol.9 P.488-495 google
  • 21. During A, Rinklebe J, Bohme F, Wennrich R, Stark H-J, Mothes S, Du Laing G, Schulz E, Neue H-U 2009 Mercury volatilization from three floodplain soils at the central Elbe River, Germany [Soil Sediment Contam: An Internat J] Vol.18 P.429-444 google doi
  • 22. Duval C, Poelman MC 1995 Scavenger effect of vitamin E and derivatives on free radicals generated by photoirradiated pheomelanin [J Pharm Sci] Vol.84 P.107-110 google doi
  • 23. 2008 Opinion of the scientific panel on contaminants in the food chain on a request from the European Commission on mercury as undesirable substance in feed [European Food Safe Author J] Vol.654 P.1-76 google
  • 24. Friedmann AS, Watzin MC, Brinck-Johnsen T, Leiter JC 1996 Low levels of dietary methylmercury inhibit growth and gonadal development in juvenile walleye (Stizostedion vitreum) [Aquat Toxicol] Vol.35 P.265-278 google doi
  • 25. Fukino H, Hirai M, Hsueh YM, Yamane Y 1984 Effect of zinc pretreatment on mercuric chloride-induced lipid peroxidation in the rat kidney [Toxicol Appl Pharmacol] Vol.73 P.395-401 google doi
  • 26. Ganther HE 1980 Interactions of vitamin E and Selenium with mercury and silver [Ann N Y Acad Sci] Vol.355 P.212-226 google doi
  • 27. Guillot I, Lohr B, Weiser H, Halbach S, Rambeck WA 1998 Influence of vitamin C on cadmium and mercury accumulation [J Anim Physiol Anim Nutr (Berl)] Vol.80 P.167-169 google doi
  • 28. Houck A, Cech JJ 2004 Effects of dietary methylmercury on juvenile Sacramento blackfish bioenergetics [Aquat Toxicol] Vol.69 P.107-123 google doi
  • 29. Kalender S, Kalender Y, Ogutcu A, Uzunhisarcikli M, Durak D, Acikgoz F 2004 Endosulfan-induced cardiotoxicity and free radical metabolism in rats: the protective effect of vitamin E [Toxicology] Vol.202 P.227-235 google doi
  • 30. Kim N-S, Lee B-K 2010 Blood total mercury and fish consumption in the Korean general population in KNHANES III, 2005 [Sci Total Environ] Vol.408 P.4841-4847 google doi
  • 31. Kung LJ, Soares JH, Haltman WA 1987 Effect of vitamin E and synthetic antioxidants on the survival rate of mercury-poisoned Japanese quail [Poult Sci] Vol.66 P.325-331 google doi
  • 32. Lee JW, De Riu N, Lee S, Bai SC, Moniello G, Hung SS 2011 Effects of dietary methylmercury on growth performance and tissue burden in juvenile green (Acipenser medirostris) and white sturgeon (A. transmontanus) [Aquat Toxicol] Vol.105 P.227-234 google doi
  • 33. Lund B-O, Miller DM, Woods JS 1993 Studies on Hg (II)-induced H2O2 formation and oxidative stress in vivo and in vitro in rat kidney mitochondria [Biochem Pharmacol] Vol.45 P.2017-2024 google doi
  • 34. Moon HB, Kim HS, Choi M, Yu J, Choi HG 2009 Human health risk of polychlorinated biphenyls and organochlorine pesticides resulting from seafood consumption in South Korea, 2005-2007 [Food Chem Toxicol] Vol.47 P.1819-1825 google doi
  • 35. Moon HB, Kim SJ, Park H, Jung YS, Lee S, Kim YH, Choi M 2011 Exposure assessment for methyl and total mercury from seafood consumption in Korea, 2005 to 2008 [J Environ Monit] Vol.13 P.2400-2405 google doi
  • 36. Nandini SD, Lata B 2010 Role of some antioxidants on mercury chloride induced spermatogenesis in swiss albino mice during pre pubertal phase of life [Indian J Sci Res] Vol.1 P.19-25 google
  • 37. 2011 Nutrient Requirements of Fish and Shrimp google
  • 38. 2005 Mineral tolerance of animals google
  • 39. Patil GR, Rao MV 1999 Role of ascorbic acid on mercuric chloride toxicity in vital organs of mice [Indian J Environ Toxicol] Vol.9 P.53-55 google
  • 40. Rambeck B, Specht U, Wolf P 1996 Pharmacokinetic interactions of the new antiepileptic drugs [Clin Pharmacokinet] Vol.31 P.309-324 google doi
  • 41. Rao MV, Sharma PSN 2001 Protective effect of vitamin E against mercuric chloride reproductive toxicity in male mice [Reprod Toxicol] Vol.15 P.705-712 google doi
  • 42. Roe A. 2003 Fishing for identity: Mercury contamination and fish consumption among indigenous groups in the United States [Bull Sci Technol Soc] Vol.23 P.368-375 google doi
  • 43. Sheweita SA. 1998 Heavy metal-induced changes in the Glutathione levels and Glutathione Reductase/Glutathione S-Transferase activities in the liver of male mice [Int J Toxicol] Vol.17 P.383-392 google
  • 44. Sies H, Stahl W, Sundquist AR 1992 Antioxidant functions of vitamins [Ann N Y Acad Sci] Vol.669 P.7-20 google doi
  • 45. Valko M, Morris H, Cronin M 2005 Metals, toxicity and oxidative stress [Curr Med Chem] Vol.12 P.1161-1208 google doi
  • 46. Wang W-X, Onsanit S, Dang F 2012 Dietary bioavailability of cadmium, inorganic mercury, and zinc to a marine fish: Effects of food composition and type [Aquaculture] Vol.356-357 P.98-104 google doi
  • 47. Weis JS 2009 Reproductive, developmental, and neurobehavioral effects of methylmercury in fishes [J Environ Sci Health C Environ Carcinog Ecotoxicol Rev] Vol.27 P.212-225 google doi
  • 48. Welsh SO 1979 The protective effect of vitamin E and N,N'-diphenylp-phenylenediamine (DPPD) against methylmercury toxicity in the rat [J Nutr] Vol.109 P.1673-1681 google
  • 49. Welsh SO, Soares JH Jr 1976 The protective effect of vitamin E and selenium aginst methylmercury toxicity in the Japanese quail. Nutrition Reports International CODEN: NURIBL 13 P.43-51 google
  • 50. Wiener JG, Krabbenhoft DP, Heinz GH, Scheuhammer AM, Hoffman DJ, Rattner BA, Burton GA, Cairns J 2003 Ecotoxicology of mercury google
  • 51. Zalups R, Lash L 1994 Recent advances in understanding the renal transport and toxicity of mercury [J Toxicol Environ Health] Vol.42 P.1-44 google doi
이미지 / 테이블
  • [ Table 1. ]  Composition of the experimental diets (% of dry matter basis)
    Composition of the experimental diets (% of dry matter basis)
  • [ Table 2. ]  Analyzed concentration of Hg, vitamin C and E of the experimental diets (mg/kg)
    Analyzed concentration of Hg, vitamin C and E of the experimental diets (mg/kg)
  • [ ] 
  • [ ] 
  • [ ] 
  • [ Table 3. ]  Growth performance of juvenile olive flounder fed experimental diet for 8 weeks*
    Growth performance of juvenile olive flounder fed experimental diet for 8 weeks*
  • [ Table 4. ]  Mercury concentrations (μg/g of wet matter basis) in muscle, liver and kidney of juvenile olive flounder fed the experimental diets for 8 weeks*
    Mercury concentrations (μg/g of wet matter basis) in muscle, liver and kidney of juvenile olive flounder fed the experimental diets for 8 weeks*
(우)06579 서울시 서초구 반포대로 201(반포동)
Tel. 02-537-6389 | Fax. 02-590-0571 | 문의 : oak2014@korea.kr
Copyright(c) National Library of Korea. All rights reserved.