Dietary Selenium and Arsenic Additions in the Life Cycle of Laying Hens

Economic losses from plants grown on seleniferous soils have been reported in the literature for the last 30-35 years. The overall magnitude of such losses will never be known, but to individual gerdsmen they often meant financial ruin. The earliest report of conditions indicative of selenium poisoning was by Madison (1856) as indicated by Franke in 1934. Selenium toxicity has attracted much attention in Wyoming and South Dakota in particular, where in several areas the soil contains unusually high levels of selenium. This element is absorbed and concentrated in various parts of plants. From there it may be further transferred into the animal’s tissues and by-products such as eggs and milk. In 1935, Franke et al. recognized selenium as the toxicant naturally occurring in certain feedstuffs which caused the malady now commonly known as “Alkali disease.” No practical protective remedies are available today for range stock except to limit grazing in certain areas or move the animals to different paces. The use of arsenicals like arsenilic acid or 3-nitro-4 4-hydroxy phenylarsonic acid has been tried to counteract the toxic effects of selenium with partial success, but the use of s=arsenicals requires careful administration. Should a safe and satisfactory means of completely preventing this toxicity in poultry be found, it might allow for the development of new areas of grain utilization in seleniferous areas. This study was undertaken to determine the effects of dietary selenium and arsenic additions over the life cycle of laying hens up to 76 weeks of age. A non-toxic level of selenium was also used to ascertain the effects of prolonged use on reproductive performance