Abstract
Arsenic is a major threat to a large part of the population due to its carcinogenic nature. The toxicity of arsenic emerges from glutathione (GSH) depletion caused by arsenic with unknown mechanism. GSH depletion leads to apoptosis, lipid peroxidation and eventual cell death. The present study was designed to provide insight into the extent of changes in GSH level by arsenic. Plasma and cytosolic fraction were investigated for determination of changes in GSH metabolic status caused by arsenic in the form of arsenic trioxide (ATO). The depletion of GSH level was found to be positively correlated with increasing parameters, that is, arsenic concentration and time of incubation. Our findings show that changes in GSH status produced by arsenic could be due to adduct (As-(SG)3) formation. This change in GSH metabolic status provides information regarding mechanism of toxicity of ATO. These findings are important for the rational design of antidote for the prevention of arsenic induced toxicity. Key words: Arsenic trioxide (ATO), glutathione (GSH), dithiobisnitrobenzoic acid (DTNB), plasma, cytosolic fraction (C.F).
Highlights
Arsenic (As) is a widespread environmental toxin
Plasma and cytosolic fraction were investigated for determination of changes in GSH metabolic status caused by arsenic in the form of arsenic trioxide (ATO)
Change in plasma-GSH level at different ATO concentrations: GSH level was determined in different plasma samples, each one having varied ATO concentrations
Summary
Arsenic (As) is a widespread environmental toxin. It enters the organisms by dermal contact, inhalation, or ingestion of contaminated drinking water and affects nearly entire organ systems of the body (Ratnaike, 2003). Nucleophilic reactivity of GSH is based on conjugation of its thiol group with electrophilic compounds (Commandeur et al, 1995). This characteristic underlies its potent antioxidant action and enzyme cofactor properties, and supports a complex thiol-exchange system, which hierarchically regulates cell activity. Oxidative stressors that can deplete GSH include ultraviolet and other radiation (Cai et al, 2000), viral infections (Kidd, 1997; Look et al, 1997), environmental toxins, household chemicals, and heavy metals (Kidd, 1997) surgery, inflammation, burns, septic shock (Luo et al, 1998; Spies et al, 1994) and dietary deficiencies of GSH precursors and enzyme cofactors (Whitcomb and Block, 1994)
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