Interactions between selenium and group Va-metalloids (arsenic, antimony and bismuth) in the biliary excretion

Gregus, Zoltán; Gyurasics, Ágnes; Koszorús, László

doi:10.1016/s1382-6689(97)10008-4

Cited by 36 publications

(15 citation statements)

References 35 publications

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“…Intramuscular injection of selenium prior to lead exposure provided prophylactic action against lead effects and we observed that selenium enhances the auto oxidant capacity of the cells by increasing the activity of the superoxide dismutase, glutathione reductase and glutathione content 115) . Interaction of arsenic and selenium promotes the biliary excretion of exogenous selenium and selenite also augments the excretion of arsenic into bile [116][117][118] . These authors suggested that arsenic augmented the hepatobiliary transport of selenium and facilitated accumulation of selenium in red blood cells.…”

Section: Seleniummentioning

confidence: 99%

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Kalia¹,

Flora²

2005

Journal of Occupational Health

267

161

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Strategies for Safe and Effective Therapeutic Measures for Arsenic and LeadPoisoning: Kiran Kalia, et al. Department of Biosciences, Sardar Patel University, IndiaExposure to toxic metals remains a widespread occupational and environmental problem in world. There have been a number of reports in the recent past suggesting an incidence of childhood lead poisoning and chronic arsenic poisoning due to contaminated drinking water in many areas of West Bengal in India and Bangladesh has become a national calamity. Low level metal exposure in humans is caused by air, food and water intake. Lead and arsenic generally interferes with a number of body functions such as the central nervous system (CNS), the haematopoietic system, liver and kidneys. Over the past few decades there has been growing awareness and concern that the toxic biochemical and functional effects are occurring at a lower level of metal exposure than those that produce overt clinical and pathological signs and symptoms. Despite many years of research, we are still far from an effective treatment of chronic plumbism and arsenicosis. Medical treatment of acute and chronic lead and arsenic toxicity is furnished by chelating agents. Chelating agents are organic compounds capable of linking together metal ions to form complex ring-like structures called chelates. They have been used clinically as antidotes for acute and chronic poisoning. 2, 3-dimercaprol (BAL) has long been the mainstay of chelation therapy for lead or arsenic poisoning. Meso 2, 3, -dimercaptosuccinic acid (DMSA) has been tried successfully in animals as well as in a few cases of human lead and arsenic poisoning. DMSA could be a safe and effective method for treating lead or arsenic poisoning, but one of the major disadvantages of chelation with DMSA has been its Review inability to remove lead from the intracellular sites because of its lipophobic nature. Further, it does not provide protection in terms of clinical/ biochemical recovery. A new trend in chelation therapy is to use combined treatment. This includes the use of structurally different chelators or a combination of an adjuvant and a chelator to provide better clinical/ biochemical recovery in addition to lead mobilization. The present review article attempts to provide update information about the current strategies being adopted for a safe, effective and specific treatment for two major toxic metals or metalloid.

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Section: Seleniummentioning

confidence: 99%

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Kalia¹,

Flora²

2005

Journal of Occupational Health

267

161

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show abstract

“…The mutual detoxification between arsenite and selenite can be rationalized in terms of the in vivo formation and subsequent biliary excretion of the seleno-bis (S-glutathionyl) arsinium ion, [(GS) 2 AsSe] À (Scheme 1). 14,16,17 In vitro studies revealed that this species is rapidly formed in blood 73 and most likely assembled inside erythrocytes 74 after individual import of arsenite and selenite into these cells. 75 Intracellular metabolism of arsenite and selenite in erythrocytes to (GS) 2 As±OH/ (GS) 3 As 76 and selenide 59,70,77,78 would then allow nucleophilic attack of the latter on the arsenic atom of (GS) 2 As±OH or (GS) 3 As to give [(GS) 2 AsSe] À .…”

Section: Effect Of Toxic Metals and Metalloids On The Metabolism Of Smentioning

confidence: 99%

Review: Reactive selenium metabolites as targets of toxic metals/metalloids in mammals: a molecular toxicological perspective

Gailer

2002

Applied Organom Chemis

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Human activities have been contaminating the environment with toxic heavy metal and metalloid compounds. Since the toxicity of one metal or metalloid can be dramatically modulated by the simultaneous ingestion of another, studies addressing the molecular basis of chemical interactions between toxic and essential elements are increasingly important. The intravenous injection of rabbits with selenite and arsenite or with selenite and mercuric mercury resulted in the in vivo formation of the seleno-bis (S-glutathionyl) arsinium ion, [(GS) 2 AsSe] À , or a glutathione-coated mercuric selenide, (GS) 5 (HgSe) core , in blood. The formation of these species (and the formation of a cadmium±selenium species in blood after the exposure of rats to selenite and cadmium) critically involves reactive selenite metabolites, such as GS±Se À and/or HSe À , which indicates that these physiologically important metabolites are molecular targets of ingested toxic metals and metalloids. The fate and stability of [(GS) 2 AsSe] À and (GS) 5 (HgSe) core in vivo imply that the chronic exposure of mammals to inorganic arsenic and mercury will cumulatively affect the bioavailability of selenium, which could lead to selenium deficiency. Since selenium deficiency is significantly associated with the etiology of cancer in humans, the GSH-driven in vivo formation of selenium-containing metal and metalloid species provides a likely molecular mechanism for the chronic toxicity of environmentally persistent inorganic arsenic, mercury and cadmium.

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“…In any case, this is not a mechanism that could not be operative here, since HOS cells show very little ability to methylate arsenite [18]. Arsenite and selenite enhance the biliary excretion of metabolites of each other [6,29], possibly through a formation of a diglutathione compound [(GS) 2 AsSe] À [30]. It is not known whether this compound forms in these cultured cells.…”

Section: Discussionmentioning

confidence: 93%

Selenium prevents spontaneous and arsenite-induced mutagenesis

Rossman

Uddin

2004

International Congress Series

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Interactions between selenium and group Va-metalloids (arsenic, antimony and bismuth) in the biliary excretion

Cited by 36 publications

References 35 publications

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Review: Reactive selenium metabolites as targets of toxic metals/metalloids in mammals: a molecular toxicological perspective

Selenium prevents spontaneous and arsenite-induced mutagenesis

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