Page 507 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition
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474 SECTION | V Metals and Micronutrients




  VetBooks.ir  and viability in rodent models (Kaur and Bansal, 2005;  understand. The small difference between deficiency and
                                                                toxicity in terms of dietary intake makes the risk of acci-
             Shalini and Bansal, 2007, 2005; Boitani and Puglisi,
                                                                dental selenium poisoning high. Many areas of the world
             2008). If other species have similar effects, this could
             negatively affect herd reproductive performance. In addi-  have seleniferous soils that can cause poisoning via
             tion, it must be noted that Se accumulates in the fetus at  ingestion of natural forages grown on them. As there is
             the expense of the dam (Puls, 1994). Thus, higher accu-  no specific treatment for selenium toxicosis, it is critical
             mulation of selenium in the fetus may result in abortions,  that appropriate education be utilized in order to mini-
             stillbirths or weak/lethargic calves. Yeager et al. (1998)  mize the risks to the livestock industry.
             reported a 7% abortion rate in a beef herd where cows  Future research needs to address the mechanisms of
             had selenium concentrations suggestive of chronic seleno-  physiologic damage caused by both acute and chronic
             sis and fetal hepatic selenium concentrations suggestive  selenium poisoning with differing chemical forms of sele-
             of toxicosis, but in a dosing study they only had one weak  nium. With an understanding of the cellular mechanisms
             calf born that died shortly after birth. Although terato-  of selenium poisoning, more specific means of treatment
             genic effects of selenium poisoning are well documented  might be developed. In addition, a clearer understanding
             in avian species, historical reports are all that are avail-  of thresholds for chronic selenium poisoning is needed.
             able for horses and sheep (Smith et al., 1936; Beath et al.,  With the knowledge that certain ruminal microbes can
             1939). However, toxic plants in the environment may  reduce various forms of selenium to nonabsorbable forms,
             have also played roles. At least some of the adverse  preventive use of these microbes in seleniferous areas to
             effects on reproduction caused by excess selenium in  prevent systemic accumulation and poisonings should be
             ruminants are caused by interference with absorption and  investigated.
             retention of copper that results in copper deficiency.
                Selenosis in poultry and other avian species has major  REFERENCES
             effects in reproduction. Poor hatchability, embryonic
             deformities and embryonic death are common sequelae to  Alexander, J., Hogberg, J., Thomassen, Y., et al., 1987. Selenium.
             selenium poisoning (Hoffman, 2002; Latshaw et al.,   In: Seiler, H.G. (Ed.), Handbook on Toxicity of Inorganic
                                                                  Compounds. Marcel Dekker, New York, p. 585.
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             TREATMENT                                          Arthur, J.R., Beckett, G.J., 1994. New metabolic roles for selenium.
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             sure. Although the maximal tolerable level for selenium  selenium supplements on the distribution of selenium among serum
             was once set at 2 mg/kg of diet per day for all species,  proteins in cattle. J. Dairy Sci. 81, 1089 1094.
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             poultry it is set at 3 mg/kg of diet, and for fish it is set at  Beath, O.A., 1937. The occurrence of selenium and seleniferous vegeta-
                                                                  tion in Wyoming. II. Seleniferous vegetation. Wyo. Agric. Exp. Sta
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                As there is no specific mechanism of chelation and
                                                                Beath, O.A., Eppson, H.F., Gilbert, C.S., 1935. Selenium and other toxic
             removal of selenium in animals, the primary treatment
                                                                  minerals in soils and vegetation. Wyo. Agric. Exp. Sta Bull.
             protocol is of supportive care with both acute and chronic
                                                                  Laramie, WY. 206, 1 55.
             selenium poisoning. With chronic poisoning, it is impor-  Beath, O.A., Eppson, H.F., Gilbert, C.S., et al., 1939. Poisonous plants
             tant to understand the long-term commitment necessary to  and livestock poisoning. Wyo. Agric. Exp. Sta Bull. 231, 1 104.
             allow an animal with hoof lesions time to regrow the hoof  Behne, D., Hillmert, H., Scheid, S., et al., 1988. Evidence for specific
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                                                                Boitani, C., Puglisi, R., 2008. Selenium, a key element in spermatogene-
                                                                  sis and male fertility. In: Cheng, C.Y. (Ed.), Molecular Mechanisms
             CONCLUDING REMARKS                                   in Spermatogenesis. Landes Bioscience and Springer Science
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                                                                Bopp, B.A., Sonders, R.C., Kesterson, J.W., 1982. Metabolic fate of
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