Advanced SearchSearch Tips
Arsenic Toxicity on Duck Spermatozoa and the Ameliorating Effect of L-Ascorbic Acid
facebook(new window)  Pirnt(new window) E-mail(new window) Excel Download
 Title & Authors
Arsenic Toxicity on Duck Spermatozoa and the Ameliorating Effect of L-Ascorbic Acid
Lin, Chai-Ching; Huang, Chia-Cherng; Chen, Ming-Cheng; Huang, Andrew Jeng-Fang; Chiou, Hung-Yi;
  PDF(new window)
The objectives of this study were to understand the possible mechanism of duck sperm toxicity induced by arsenic exposure in vivo, and to investigate the roles of the antioxidant L-ascorbic acid in ameliorating the arsenic-induced sperm impairment. To test the acute toxicity, the percentages of mortality of mature drakes treated with different concentrations of trivalent sodium arsenite, As (III), and pentavalent sodium arsenate, As (V) were measured. The LD50 value of As (III) for mature drakes was ppm. Although As (V) didn't cause any deaths even at a concentration of 40 ppm, the chronic toxicity of As (V) on sperm quality was shown by a decreased fertilization rate. When the concentrations of As (V) were above 0.4 ppm, fertilization rates were lower than those of 0.04 ppm and control. Drakes treated with 40 ppm of As (V) had the highest malondialdehyde (MDA) level in the testis tissue, testis. This showed that 40 ppm of As (V) significantly induced lipid peroxidation in testis tissue. For the 1.2 ppm As (III) treatment, several significant effects were observed: (1) sperm motility was decreased most dramatically by % after three days of incubation; (2) fertilization rate of artificially inseminated semen was the lowest, ; (3) the MDA concentration in testis tissue, testis, was significantly higher than the others (p<0.05); (4) the sperm number, , was significantly lower than with the 60 ppb and control treatments (p<0.05); (5) a black appearance and soft texture was observed in the testis tissue. The antioxidant L-ascorbic acid administered along with 1.2 ppm As (III) decreased the toxicity of arsenic. The ameliorating effects included: improved sperm motility, increased sperm number and fertilization rate, and decreased MDA concentration in the testis tissue. This study suggests that the toxicity of the trivalent arsenic on sperm quality is partly from free radicals generated by its metabolic pathway, and the antioxidant ascorbic acid ameliorates arsenic-caused sperm impairment.
Drake;Sperm Quality;Antioxidant;Ascorbic Acid;Fertilization Rate;LD50;Lipid Peroxidation;
 Cited by
Review on arsenic-induced toxicity in male reproductive system and its amelioration, Andrologia, 2017, 49, 9, e12791  crossref(new windwow)
Aitken, R. J., D. Buckinhham and D. Harkiss. 1993. Use of xanthine oxidase free radical generating system to investigate the cytotoxic effects of reactive oxygen species on human spermatozoa. J. Reprod. Fertil. 97:441-450. crossref(new window)

Aitken, R. J. and J. S. Clarkson. 1987. Cellular basis of defective sperm function and its association with the genesis of reactive oxygen species by human spermatozoa. J. Reprod. Fertil. 81:459-469. crossref(new window)

Alvarez, J. G., J. C. Touchstone, L. Blasco and B. T. Storey. 1987. Spontaneous lipid peroxidation and production of hydrogen peroxide and superoxide in human spermatozoa. Superoxide dismutase as major enzyme protectant against oxygen toxicity. J. Androl. 8:338-348. crossref(new window)

Anke, M., G. Hoffmann, M. Grn, B. Groppel and E. Riedel. 1982. IAEA-TEC DOC 267:135-146.

Baxley, M. N., R. D. Hood, G. C. Vedel, W. P. Harrison and G. M. Szczech. 1981. Bull. Environ. Contam. Toxicol. 26:749-756. crossref(new window)

Beaudoin, A. R. 1974. Teratology 10:153-156. crossref(new window)

Blair, P. C., M. B. Thompson, B. Bechtold, R. E. Wilson, M. P. Moorman and B. A. Fowler. 1990. Evidence for oxidative damage to red blood cells in mice induced by arsine gas. Toxicol. 63:25-24. crossref(new window)

Brown, K. G. and C. J. Chen. 1994. Observed dose-response for internal cancers and arsenic in drinking water in the blackfoot disease endemic region of Taiwan. In: Arsenic Exposure and Health (Ed. W. R. Chappell, C. O. Abernathy and C. R. Cothern). Science and Technology Letters. Northwood. pp. 153-170.

Chang, W. C., S. H. Chen, H. L. Wu, G. Y. Shi, S. Murota and I. Morita. 1991. Cytoprotective effect of reduced glutathione in arsenic-induced endothelial cell injury. Toxicol. 69:101-110. crossref(new window)

Charbonneau, S. M., G. K. H. Tam, F. Bryce, Z. Zawidzka and E. Sandi. 1979. Toxicol. Lett. 3:107-113. crossref(new window)

Chen, C. J. 1980. Blackfoot disease. Lancet. 336:442. crossref(new window)

Chen, C. J., C. W. Chen, M. M. Wu and T. L. Kuo. 1992. Cancer potential in liver, lung, bladder and kidney due to ingested inorganic arsenic in drinking water. Br. J. Cancer 66:888-892. crossref(new window)

Chen, C. J. and L. J. Lin. 1994. Human carcinogenicity and atherogenicity induced by chronic exposure to inorganic arsenic. In: Advances in Environmental Science and Technology: Arsenic in Environment. Part II: Human health and ecosystem effects (Ed. J. O. Nriagu). John Wiley & Sons, Ins., New York. 27:109-131.

Chen, C. J., T. L. Kuo and M. M. Wu. 1988. Arsenic and cancers. Lancet. 1:414-415. crossref(new window)

Chen, C. J., Y. C. Chuang, T. M. Lin and H. Y. Wu. 1985. Malignant neoplasms among residents of a blackfoot diseaseendemic area in Taiwan: High arsenic artesian well water and cancers. Cancer Res. 45:5895-5899.

Chen, C. J., Y. C. Chuang, S. L. You, T. M. Lin and H. Y. Wu. 1986. A retrospective study on malignant neoplasms of bladder, lung and liver in blackfoot disease-endemic area in Taiwan. Br. J. Cancer 53:399-405. crossref(new window)

Esterbauer, H., R. J. Schaur and H. Zollner. 1991. Chemistry and biochemistry of 4-hydroxynonenal, malondialdehyde and related aldehydes. Free Rad. Biol. Med. 11:81-128. crossref(new window)

Farmer, J. G. and L. R. Johnson. 1990. Assessment of occupational exposure to inorganic arsenic based on urinary concentrations and speciation of arsenic. Br. J. Ind. Med. 47:342-348.

Ferm, V. H. and L. Kilham. 1977. Environ. Res. 14:483-486. crossref(new window)

Griveau, J. F., P. Renard and D. LeLannou. 1994. An in vitro promoting role for hydrogen peroxide in human sperm capacitation. Int. J. Androl. 17:300-307. crossref(new window)

Guo, H. R., C. J. Chen and H. L. Greene. 1994. Arsenic in drinking water cancers: a brief descriptive review of Taiwan studies. In: Arsenic Exposure and Health (Ed. W. R. Chappell, C. O. Abernathy and C. R. Cothern) Science and Technology Letters. Northwood. pp. 129-138.

Hollins, J. G., S. M. Charbonneau, F. Bryce, J. M. Ridgeway, G. K. H. Tam and R. F. Will. 1979. Toxicol. Lett. 4:7-13. crossref(new window)

Hood, R. D. and W. P. Harrison. 1982. Bull. Environ. Contam. Toxicol. 29:671-678. crossref(new window)

Huang, H., C. F. Huang,, D. R. Wu, C. M. Jinn and K. Y. Jan. 1993. Glutathione as a cellular defense against arsenite toxicity in cultured Chinese hamster ovary cells. Toxicol. 79:195-204. crossref(new window)

IARC (International Agents for Research on Cancer) 1980. Carcinogenesis of arsenic and arsenic compounds. IARC Monogr. 23: 37-141.

Ishinishi, N., K. Tsuchiya, M. Vahter and B. A. Fowler. 1986. Arsenic. In: Handbook on the Toxicology of Metals (Ed. L. Friberg, G. F. Nordberg and V. Vouk) Elsevier Science Publishers. Amsterdam. pp. 43-83.

Iwasaki, A. and C. F. Gagnon. 1992. Formation of reactive oxygen species in spermatozoa of infertile patients. Fertil. Steril. 57(2):409-416. crossref(new window)

Keyse, S. M. and R. M. Tyrrell. 1989. Heme oxygenase is the major 32-kDa stress protein induced in human skin fibroblasts by UVA radiation, hydrogen peroxide, and sodium arsenite. Proc. Natl. Acad. Sci. USA 86:99-103. crossref(new window)

Lakso, J. and S. A. Peoples. 1975. Aric. Biol. Chem. 44:1993-1994.

Lee, T. C. and I. C. Ho. 1994. Expression of heme oxygenase in arsenite-resistant human lung adenocarcinoma cells. Cancer Res. 54:1660-1664.

Lee, T. C. and I. C. Ho. 1995. Modulation of cellular antioxidant defense activities by sodium arsenite in human fibroblasts. Arch. Toxicology 69:498-504. crossref(new window)

Lee, T. C., M. Oshimura and J. C. Barrett. 1985. Comparison of arsenic-induced cell transformation, cytotoxicity, mutation and cytogenetic effects in Syrian hamster embryo cells in culture. Carcinogenesis 6:1421-1426. crossref(new window)

Lee, T. C., W. J. Wei, W. J. Chang,, I. C. Ho, J. F. Lo, K. Y. Jan and H. Huang. 1989. Elevation of glutathione levels and glutathione S-transferase activity in arsenic-resistant Chinese hamster ovary cells. In Vitro Cell Dev. Biol. 25:442-448. crossref(new window)

Leonard, A. and R. R. Lauwerys. 1980. Carcinogenicity, teratogenicity and mutagenicity of arsenic. Mutat. Res. 75:49-62. crossref(new window)

Lindgren, A., B. R. G. Danielsson, L. Dencker and M. Vahter. 1984. Acta. Pharmacol. Toxicol. 54:311-320. crossref(new window)

Marafante, E., J. Rade, R. Pietra, E. Sabbioni and F. Bertolero. 1980. In: Arseni. 3. Spurenelement-Symposium (Ed. M. Anke, H. J. Schneider and C. Bruckner). Wiss. Publ., Friedrich-Schiller-Univ., Jena, G.D.R. pp. 49-55.

Nordenson, I. and L. Beckman. 1991. Is the genotoxic effect of arsenic mediated by oxygen free radicals? Hum. Hered. 41:71-73. crossref(new window)

Odanaka, Y., O. Matano and S. Goto. 1980. Bull. Environ. Contam. Toxicol. 24:452-459. crossref(new window)

Oehninger, S., P. Blackmore, M. Mahony and G. Hodgen. 1995. Effects of hydrogen peroxide on human spermatozoa. J. Assisted Reprod. Genetics 12(1):41-47. crossref(new window)

Tseng, C. H., C. J. Chen, B. J. Lin and T. Y. Tai. 1994. Abnormal response of ankle pressure after exercise in seemingly normal subjects living in blackfoot disease-hyperendemic villages in Taiwan. Vascular Surg. 28:607-617. crossref(new window)

Tseng, W. P. 1977. Effects and dose-response relationships of skin cancer and blackfoot disease with arsenic. Environ. Health. Perspect. 19:109-119. crossref(new window)

Tseng, W. P. 1989. Blackfoot disease in Taiwan: A 30 year followup. Angiology 40:547-558. crossref(new window)

Tseng, W. P., H. M. Chu and S. W. How. 1968. Prevalence of skin cancer in an endemic area of chronic arsenicism in Taiwan. J. Natl. Cancer. Inst. 40:453-463.

Vahter, M. and J. Envall. 1983. Environ. Res. 32:14-24. crossref(new window)

Vodela, J. K., S. D. Lenz, J. A. Renden, W. H. Mcelhenney and Kemppainen. 1997. Drinking water contaminants (arsenic, cadmium, lead, benzene, and trichloroehtylene). 2. Effects on reproductive performance, egg quality, and embryo toxicity in broiler breeders. Poult. Sci. 76:1493-1500. crossref(new window)

Wang, T. S. and H. Huang. 1994. Active oxygen species are involved in the induction of micronuclei by arsenic in XRS-5 cells. Mutagenesis 9:253-257. crossref(new window)

Wu, M. M., T. L. Kuo, Y. H. Huang and C. J. Chen. 1989. Doseresponse relationship between arsenic concentration in well water and mortality from cancers and vascular disease. Am. J. Epidemiol. 130:1123-1132. crossref(new window)

Yamanaka, K., A. Hasegawa, R. Sawamura and S. Okada. 1991. Cellular response to oxidative damage in lung induced by the administration of dimethylarsinic acid, a major metabolite of inorganic arsenics, in mice. Toxicol. Appl. Pharmacol. 108:205-213. crossref(new window)

Yamanaka, K., A. Hasegawa, R. Sawamura and S. Okada. 1989a. DNA Strand breaks in mammalian tissue induced by methylarsenics. Biol. Trace. Elem. Res. 21:413-417. crossref(new window)

Yamanaka, K., A. Hasegawa, R. Sawamura and S. Okada. 1989b. Dimethylated arsenics induce DNA strand breaks in lung via the production of active oxygen in mice. Biochem. Biophys. Res. Commun. 165:43-50. crossref(new window)

Yamanaka, K., M. Hoshino, M. Okamoto, R. Sawamura, A. Hasegawa and S. Okada. 1990. Induction of DNA damage by dimethylarsine, a metabolite of inorganic arsenics, is for the major part likely due to its peroxyl radical. Biochem. Biophys. Res. Commun. 168:58-64. crossref(new window)