Selenium compounds, acute toxicity

In domestic and experimental animals, renal effects have been observed following both acute and chronic oral exposures to selenium compounds. Administration of a single oral (subroute not specified) dose of sodium selenite at 5 mg selenium/kg/day produced hydropic degeneration of the kidney in sheep (Smyth et al. 1990). In a study of the toxicity of L-selenomethionine to long-tailed macaques by nasogastric intubation, two animals administered 0.24 mg selenium/kg/day aspirated vomitus secondary to emesis, developed obvious gastritis, and died of anorexia, one after 10 days and the other after 15 days of... 

Selenium is primarily eliminated in the urine and feces in both humans and laboratory animals. The distribution of selenium between the two routes seems to vary with the level of exposure and time after exposure. The form of selenium excreted is dependent on the form of selenium that was ingested. In cases of acute exposure to toxic concentrations of selenium or selenium compounds, significant amounts of selenium can be eliminated in the breath, causing the characteristic "garlic breath."... 

Little is known about the specific biochemical mechanism(s) by which selenium and selenium compounds exert their acute toxic effects. Long-term effects on the hair, skin, nails, liver, and nervous system are also well documented, and a general theory has been developed to explain the toxicity of exposure to excess selenium, as discussed below. Generally, water-soluble forms are more easily absorbed and are generally of greater acute toxicity. Mechanisms of absorption and distribution for dermal and pulmonary uptake are unknown and subject to speculation, but an active transport mechanism for selenomethionine absorption in the intestine has been described (Spencer and Blau 1962). The mechanisms by which selenium exerts positive effects as a component of glutathione peroxidase, thioredoxin reductase, and the iodothyronine 5 -deiodinases are better understood, but the roles of other selenium-containing proteins in mammalian metabolism have not been clarified. 

Data are available for acute inhalation exposures for a few of the volatile selenium compounds that have resulted in the death of animals. These exposures also produced signs of central nervous system toxicity, lung injury, and possible damage to heart and liver. No studies were located concerning health effects in animals following intermediate or chronic inhalation exposures to volatile selenium compounds or selenium dust. 

Paul and coworkers (1989) have investigated the antidotal actions of several compounds on the acute toxicity of selenium in rats. Male Wistar rats were injected sodium [ Sejselenite subcutaneously in this study. Intraperitoneal administration of diethyldithiocarbamate or treatment with citrate salt of bismuth, antimony, or germanium, administered subcutaneously, reduced selenium-induced loss of body weight in the animals. Germanium citrate and bis(carboxyethyl)germanium sesquiox-ide promoted increases in the 24-hour urinary excretion of selenium when administered 15 minutes after sodium selenite. 

Prophylactic induction of enzymes involved in the conjugation of xenobiotics reduced or prevented the acute toxic effects of T-2 toxin in the rat, while inhibition of these enzymes resulted in a higher toxicity for this trichothecene.96 Pretreatment with flavonoids,97 ascorbic acid,98 vitamin E," selenium,100 or chemoprotective compounds such as emetine101 that block trichothecene-cell association all reduce acute toxicity of these mycotoxins. However, none of these chemoprotective treatments have undergone extensive efficacy studies to evaluate their ability to protect against an aerosol or dermal exposure to trichothecene mycotoxins. 

The industrial hazards of Se were recognized in 1945 [41], Since then many cases of acute and chronic selenosis in humans via consumption of selenium compounds or by inhalation have been recorded [7,42], It is, however, interesting to note that in areas of the United States where chronic selenosis has occurred among livestock there have been no clear-cut cause-effect relationships in terms of toxicity for human health [43]. 

Selenium (Se), an essential trace element, has a protective effect against Hg toxicity. Coadministration of a selenium compound with Hg " resulted in remarkable depression of acute toxicity of Hg " through the formation of stable complexes of Hg and Se in various tissues such as liver and kidney (Naganuma and Imura 1980a, 1981, 1984a). 

Table 4. Acute toxicity of some selenium compounds [33]...

---