Abstract

In studies on the toxicity of selenium we have found marked pulmonary edema in dogs following the intravenous injection of sodium selenite equivalent to 1.83 mg. of selenium per kg., and in rats following intraperitoneal injections equivalent to 3.7 mg. of selenium per kg. As these findings on dogs and rats, and the various published observations on the volatile odoriferous compounds in the expired air from man and other mammals which have received small quantities of selenium, direct attention to the lungs in selenium poisoning, a series of studies on selenium poisoning in gill-breathing fishes has been made. One hundred fifty goldfish (average length circa 80 mm.) were carried in individual glass jars each containing 4 liters of well aerated tap water to which known quantities of sodium selenite were added. Analyses at frequent intervals showed that the quantities of sodium selenite used made no appreciable changes in the dissolved oxygen, pH, or conductivity of the water. Each fish was changed to fresh seleniferous water every 48 hours and fed 3 standard pellets of shrimp meal immediately after being transferred. In waters containing 2 parts per million of selenium the fish showed no symptoms or distress for the first 8 days, taking their food promptly. On the 8th day of exposure to 2 ppm. of selenium the fish began to refuse food, or if food were taken to regurgitate it quickly. This reaction was followed by marked anorexia for a period of several days. The first fish in this series died on the 18th day of exposure to 2 ppm. of selenium and deaths became progressively more frequent between the 25th and 37th days of the experiments, the longest survival being 46 days. The onset of anorexia always marked the beginning of the fatal phase of selenium poisoning. During the next few days the fish frequently showed inco-ordination and a definite disturbance of equilibrium and as the poisoning progressed became more lethargic and feeble. These changes in behavior were not due to lack of food alone, for these symptoms did not develop in a comparable unfed control series of fish not exposed to selenium. In other tests in which the surrounding water carried 5 ppm. of selenium goldfish died in from 4 to 10 days, the sequence of poisoning being the same as in 2 ppm. series. The goldfish experiments showed that selenium could be taken up in cumulatively lethal quantities by fish from the surrounding water. As the actual selenium intake was not determined in the goldfish series, known quantities of sodium selenite (in a 0.5% solution or less) were injected intraperitoneally into 550 catfish, Ictalurus punctatus, averaging 160 mm. in length and 54 gm. in weight. Control fish given comparable injections of physiological saline developed no symptoms and remained healthy throughout the tests. All fish were bathed in salt solution immediately after each handling to prevent fungus infections, and held out-of-doors (these experiments were conducted at Ft. Worth, Texas) in concrete hatchery raceways through which unpolluted water flowed continuously. Two types of reactions were obtained from single injections of sodium selenite, namely, acute and delayed. Sodium selenite in excess of circa 3 mg. of selenium per kg., i. e., 0.15 mg. of selenium per fish was fatal in less than 48 hours, usually in less than 7 hours at water temperature around 10°C. The toxicity of the selenite increased markedly with temperature as 0.35 mg. of selenium per kg., i. e., 0.018 mg. per fish killed in 24 hours or less at 27°C. Fish dying from acute selenium poisoning consistently showed contraction of the dermal chromatophores, so that fish receiving selenium injections were definitely lighter in color often for several hours before death than control fish receiving comparable quantities of physiological saline. This reaction of the chromatophores was readily produced locally on any part of the body by subcutaneous injections of selenite. Shortly before death the poisoned fish developed incoordination and often made spasmodic movements.

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