Selenium effects on drug and foreign compound toxicity

Combs, Gerald F.; Combs, Stephanie B.

doi:10.1016/0163-7258(87)90068-4

Cited by 13 publications

(3 citation statements)

References 45 publications

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“…Environmental cofactors could include toxic and infectious agents. Selenium deficiency has been shown to increase the toxicity of several drugs and other foreign compounds, such as nitrofurantoin and paraquat 18. Besides the established role of coxsackievirus in Keshan disease in humans, a series of studies has shown that selenium deficiency is implicated as a pathogenic factor in a number of viral infections.…”

Section: Discussionmentioning

confidence: 99%

Skeletal muscle disorders associated with selenium deficiency in humans

Chariot

Bignani²

2002

Muscle and Nerve

118

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Skeletal muscle disorders manifested by muscle pain, fatigue, proximal weakness, and serum creatine kinase (CK) elevation have been reported in patients with selenium deficiency. The object of this report was to review the conditions in which selenium deficiency is associated with human skeletal muscle disorders and to evaluate the importance of mitochondrial alterations in these disorders. A systematic literature review using the Medline database and Cochrane Library provided 38 relevant articles. The main conditions associated with selenium deficiency fell into three categories: (1) insufficient selenium intake in low soil-selenium areas; (2) parenteral or enteral nutrition, or malabsorption; and (3) chronic conditions associated with oxidative stress, such as chronic alcohol abuse and human immunodeficiency virus (HIV) infection. In low soil-selenium areas, reversibility of muscle symptoms was similar after selenium supplementation and placebo administration, suggesting a role for other factors in the development of disease. In parenteral or enteral nutrition, or malabsorption, muscle symptoms improved after selenium supplementation in 18 of 19 patients (median delay: 4 weeks). The reason that only a minority of selenium-deficient patients present with skeletal muscle disorders is unclear and is possibly related to cofactors, such as viral infections and drugs. Prospective studies of selenium-deficient myopathies would be useful in critically ill patients, alcohol abusers, and HIV-infected patients.

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Section: Discussionmentioning

confidence: 99%

Skeletal muscle disorders associated with selenium deficiency in humans

Chariot

Bignani²

2002

Muscle and Nerve

118

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“…Selenium deficiency increases toxicity of the compounds generating active oxygen species during their oxidative metabolism. On the other hand, selenium supplementation to selenium-adequate animals can protect them from toxic effects of these compounds (Combs and Combs 1987). This element also modifies a variety of immune responses (Spallholz et al 1990).…”

Section: Introductionmentioning

confidence: 97%

Modulation of procainamide toxicity by selenium-enriched yeast in rats

et al. 1993

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Free radical processes are proposed to play a crucial role in the development of procainamide adverse effects. Therefore, selenium, as a potent antioxidant, may modified procainamide toxicity. To test this hypothesis plasma and liver thiobarbituric acid-reacting substances (TBARS), plasma antioxidant activity (AOA), erythrocyte and liver superoxide dismutase (SOD), catalase, as well as selenium-dependent glutathione peroxidase (Se-GPX) were determined in the following four groups of rats: selenium-treated (Se), procainamide-treated (P), procainamide and selenium-treated (P + Se), and control (C). Morphological studies of leukocytes [tested for lupus erythematosus (LE) cells] and liver were also made. Atypical, i.e. enlarged and swollen, leukocytes resulting from procainamide and selenium treatment were observed. These changes were found in four out of five rats in the Se group, eight out of ten in the P group, and in seven out of ten in the P + Se group. LE-like cells were observed in two rats in the P + Se group. A statistically significant decrease in plasma and liver TBARS by 20% and 36%, respectively, increased activity of SOD by 20%, catalase by 48% and Se-GPX by 15% in erythrocytes, and decreased activity of liver SOD by 17% and catalase by 22% were found in the P + Se group as compared to the P group. These results indicated that selenium exerted antioxidant effects on the procainamide-treated rats. However, selenium did not prevent the development of disturbances in leukocyte morphology, on the contrary, it possibly promoted the conversion of leukocytes to LE cells.

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“…The metabolism of some organic and inorganic exogenous com pounds is influenced by the selenium status. Selenium deficiency exacerbates the toxicity of several xenobiotics [3] that are potentially toxic to the system and must be "detoxified' by reactions that render them less reactive or more water-soluble. Similarly, selenium sup plementation has been found to alleviate the toxic effects of drugs and chemical carcino gens [3], Reports are available that such an effect may be mediated by xenobiotic-metabolizing enzymes in the hepatic cells, particu larly the thiol-containing ones [4] and also the UDP glucuronyl transferase [5], Taking into account the above facts, this study attempts to determine whether seleni um can bring about cell survival in hosts bear ing a rapidly growing tumor, by monitoring the xenobiotic transformation enzymes and thereby to understand the phase/phases of the neoplastic process at which selenium exerts its maximal action in offering protection.…”

Section: =1mentioning

confidence: 99%

Selenomethionine in the Inhibition of a Transplantable Murine Lymphoma: Reflection on Hepatic Drug Metabolizing Enzymes

Rana

Sardar²,

Chatterjee³

1996

Tumor Biol

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This study attempts to determine whether selenomethionine treatment can improve the survival time of mice inoculated with Dalton’s lymphoma (DL) and thereby to identify phase/ phases of the neoplastic processes at which selenium exerts its maximal action as an anticancer agent. Accordingly, a maximum of 30.76 and 143% increase in survival was brought about by treatment of selenomethionine prior to lymphoma transplantation, in comparison to mice receiving selenome-thione supplementation concurrently with inoculation of DL, and those tumor-bearing mice receiving no supplementation, respectively. Beneficiality of selenomethionine has also been studied by monitoring the continuous changes brought about by this compound on hepatic total cytochrome P-450 and bs content, NADPH cytochrome c reductase, UDP glucuronyl transferase and glutathione S-transferase (GST) activities. These are important biotransformation enzymes and are altered significantly in neoplasia. The drastic increase in all the markers studied, excepting GST, was effectively counteracted by selenomethionine treatment (more before than concurrently), which sufficiently delayed and controlled the increase in those xenobiotic indices. The 112 and 78.78% induction in GST activity brought about by prior and concurrent treatment of selenomethionine, respectively, confirms the fact that in-ducers of GSTs are often antitumorigenic.

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Selenium effects on drug and foreign compound toxicity

Cited by 13 publications

References 45 publications

Skeletal muscle disorders associated with selenium deficiency in humans

Skeletal muscle disorders associated with selenium deficiency in humans

Modulation of procainamide toxicity by selenium-enriched yeast in rats

Selenomethionine in the Inhibition of a Transplantable Murine Lymphoma: Reflection on Hepatic Drug Metabolizing Enzymes

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