Effect of selenium on vanadium toxicity in different regions of rat brain

Haider, Syed Saleem; Abdel-Gayoum, A A; El-Fakhri, Mustafa; Ghwarsha, K

doi:10.1177/096032719801700104

Cited by 28 publications

(33 citation statements)

References 18 publications

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“…A fall in the alkaline phosphatase activity may be attributed to the displacement of Mg 2 + by VO 2 + because its size resembles with Mg 2+ . These findings are substantiated by various authors (Johari et al, 2002;Haider et al, 1998;Nechay, 1984). Inhibition in adenosine triphosphatase pattern is due to the unphosphorylated enzyme which interferes with metal ion.…”

Section: Discussionsupporting

confidence: 74%

“…Selenoproteins are generally known to concentrate in cytosol of animal tissues and have a role in immune response and liver cirrhosis in human body. This protects neuronal cells against neurotoxic effects of vanadium by maintaining the availability of antioxidant nonprotein sulphydryl groups (Haider et al, 1998).The protective mechanism could be attributed due to the competition between selenium and vanadium for binding with the functional proteins and bioligand or active tissue sites or the formation of a reversible compound, metal-selenite thus reducing the availability of "free" concentration of toxic metals ions in the body might be a possible mechanism for the observed antagonism between Vanadium and Se. Thus T+Se was most effective and prevented oxidative degradation of biological membrane by catalyzing the donation of hydrogen atom from reduced glutathione.…”

Section: Discussionmentioning

confidence: 99%

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Effect of Tiron and Its Combination With Nutritional Supplements Against Vanadium Intoxication in Female Albino Rats

2007

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-In the present study an attempt has been made to evaluate the effect of Tiron along with Zinc, Selenium and Vitamin E against vanadium intoxication in female albino rats. Toxicant caused significant increase in the activities of serum transaminases, serum alkaline phosphatase and lactate dehydrogenase. Significant decrease was observed in blood sugar, serum albumin and triglyceride levels whereas serum proteins, cholesterol and urea levels increased significantly during toxicity (p ≤ 0.001). Hepatic lipid peroxidation increased significantly, whereas significant depletion was observed in reduced glutathione after vanadium administration. The activity of glucose-6-phosphatase in the liver was also inhibited significantly after vanadium administration. A significant rise was observed in glycogen content of liver and kidney after toxicant exposure. Activities of alkaline phosphatase, adenosine triphosphatase and succinic dehydrogenase were inhibited significantly on the contrary activity of acid phosphatase elevated in kidney. Histopathological examination of the liver and kidney using light and ultramicroscopic study also substantiated the above findings. It was found that therapy with Tiron was effective but significant recovery in all the parameters was found with Tiron + Se followed by Tiron+ VitE and Tiron +Zn.

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Section: Discussionsupporting

confidence: 74%

Section: Discussionmentioning

confidence: 99%

Effect of Tiron and Its Combination With Nutritional Supplements Against Vanadium Intoxication in Female Albino Rats

2007

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“…It was shown that simultaneous administration of selenium dioxide (0.02 mg Se/kg b.w.) to metavanadate-exposed rats prevented adverse V-induced action (Haider et al 1998). Se was also demonstrated to produce beneficial effects in conjunction with a therapeutic agent, Tiron (Shrivastava et al 2007).…”

Section: Selenium Interactions With Vanadiummentioning

confidence: 95%

“…In the available literature, there are only few reports investigating the biological interactions between Se and V. The in vivo study regarding the effects of selenium dioxide (SeO 2 ) on metavanadate-induced toxicity was performed by Haider et al (1998). The researchers treated rats intraperitoneally with sodium metavanadate (1.5 mg vanadium/kg b.w.)…”

Section: Selenium Interactions With Vanadiummentioning

confidence: 99%

Selenium interactions and toxicity: a review

2011

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Selenium is an essential trace element for mammals. Through selenoproteins, this mineral participates in various biological processes such as antioxidant defence, thyroid hormone production, and immune responses. Some reports indicate that a human organism deficient in selenium may be prone to certain diseases. Adverse health effects following selenium overexposure, although very rare, have been found in animals and people. Contrary to selenium, arsenic and cadmium are regarded as toxic elements. Both are environmental and industrial pollutants, and exposure to excessive amounts of arsenic or cadmium can pose a threat to many people's health, especially those living in polluted regions. Two other elements, vanadium and chromium(III) in trace amounts are believed to play essential physiological functions in mammals. This review summarizes recent studies on selenium interactions with arsenic and cadmium and selenium interactions with vanadium and chromium in mammals. Human studies have demonstrated that selenium may reduce arsenic accumulation in the organism and protect against arsenic-related skin lesions. Selenium was found to antagonise the prooxidant and genotoxic effects of arsenic in rodents and cell cultures. Also, studies on selenium effects against oxidative stress induced by cadmium in various animal tissues produced promising results. Reports suggest that selenium protection against toxicity of arsenic and cadmium is mediated via sequestration of these elements into biologically inert conjugates. Selenium-dependent antioxidant enzymes probably play a secondary role in arsenic and cadmium detoxification. So far, few studies have evaluated selenium effects on chromium(III) and vanadium actions in mammals. Still, they show that selenium may interact with these minerals. Taken together, the recent findings regarding selenium interaction with other elements extend our understanding of selenium biological functions and highlight selenium as a potential countermeasure against toxicity induced by arsenic and cadmium.

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“…Vanadium emission from human industrial activities has been estimated to comprise about 53% of total atmospheric vanadium (Hope 1994). A major source of vanadium toxicity remains the burning of fossil fuels in the Arabian Gulf (Haider et al 1998) and the Niger Delta region of Nigeria (Igado et al 2008) where massive incidental and or intentional burning of vanadium containing fuels results in pollution of confined ecosystems.…”

Section: Introductionmentioning

confidence: 99%

The Mechanism of Vanadium-Mediated Developmental Hypomyelination Is Related to Destruction of Oligodendrocyte Progenitors Through a Relationship with Ferritin and Iron

et al. 2010

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The second post-natal week in rat is the period of the most intense oligodendrocyte development and myelination. This period coincides with peak iron import by oligodendrocytes. During that time oligodendrocyte progenitors (OPCs) are sensitive to agents that may disturb normal iron homeostasis and assimilation of iron into these cells. One mechanism by which iron homeostasis can be disrupted is by environmental exposure to other metals. Vanadium is a transition metal, and exposure to vanadium during early brain development produces hypomyelination with variety of related neuro-behavioral phenotypes. In the current study, we investigated mechanisms of hypomyelination induced by vanadium exposure in developing rat brain. We demonstrate that both in vivo and in vitro, OPCs are more sensitive to vanadium exposure than astrocytes or mature oligodendrocytes. Vanadium exposure in OPCs resulted in increased ROS generation and increased annexinV labeling suggestive of apoptosis. Because ferritin is a major iron delivery protein for oligodendrocytes, we exposed the cells to recombinant ferritin and iron both of which exacerbated vanadium cytotoxicity, while the iron chelator desferroxamine (DFO) prevented cytotoxic/apoptotic effects of vanadium. To illustrate relationship between ferritin and vanadium, we demonstrate that vanadium exacerbated DNA nicking produced by iron-rich spleen ferritin, but not iron-poor apoferritin, resulting in a single and double strand breaks in a DNA relaxation assay. We propose that developmental exposure to vanadium interferes with normal iron assimilation into oligodendrocytes resulting in oxidative stress and apoptosis. Therefore, depletion of OPCs due to vanadium exposure in early post-natal period may be an important mechanism of vanadium-induced hypomyelination.

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Effect of selenium on vanadium toxicity in different regions of rat brain

Cited by 28 publications

References 18 publications

Effect of Tiron and Its Combination With Nutritional Supplements Against Vanadium Intoxication in Female Albino Rats

Effect of Tiron and Its Combination With Nutritional Supplements Against Vanadium Intoxication in Female Albino Rats

Selenium interactions and toxicity: a review

The Mechanism of Vanadium-Mediated Developmental Hypomyelination Is Related to Destruction of Oligodendrocyte Progenitors Through a Relationship with Ferritin and Iron

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