NAC and Se Protect Oxidative Stress Induced by Mercury Poisoning

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(Last Updated On: October 21, 2017)
Mercury poisoning in liver

The given set of figures represents physiological changes in liver from group 1 to 4 respectively. Images: Joshi et al., 2013

Mercury is a bivalent, stable element which, when incorporated into the living organism, causes mercury poisoning. It is the second most common cause of metal poisoning. Most of the elemental mercury, released from the industries get oxidized to bivalent mercury ion (mercuric ion or  Hg++). Thus, formed mercuric ions enter the terrestrial as well as aquatic environments through deposition. Inorganic mercury compounds have a great affinity for the thiol group (-SH or sulfhydryl group) present in the protein and other biomolecules containing cysteine.

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As mercury compounds are present in oxidized form (Hg++), they tend to oxidize other biomolecules. During these processes, varieties of reactive oxygen species are generated, causing oxidative stress (mediated by mercury poisoning). Uncontrolled production of ROS caused by inorganic mercury compounds causes severe kidney damage, neurological problems, immunological diseases etc.

According to a recent study, carried out by a team of researchers from Gorakhpur University, Gorakhpur, UP, India and Jiwaji University, Gwalior, MP, India, selenium either alone or in combination with an N-acetyl Cysteine can be used against acute mercuric chloride poisoning to minimize the oxidative stress.



They took 30 rats and divided into 5 groups (6 in each group). Rats of group 1 were taken as a control and group 2-5 were administered mercuric chloride. They took group 2 as an experimental control while they administered N-acetyl cysteine, selenium and a combination of N-acetyl cysteine and selenium to the rats of group 3, 4 and 5 respectively.

In control administered with mercuric chloride, HgCl2 caused severe physiological problems like increase in serum level of Alanine Aminotransferase (ALAT/SGPT), Aspartate Aminotransferase (ASAT/SGOT), Alkaline Phosphatase (ALP), Lactate Dehydrogenase (LD), γ-Glutamyl Transpeptidase (γ-glutamyl transferase of GGT), Cholesterol, Triglycerides, Albumin, Bilirubin, protein, urea, etc.



It was also found that these rats accumulated mercuric chloride much higher in tissues like kidney and liver as compared to other tissues. Due to which a significant rise in the lipid peroxidation level was also observed with concomitant decrease in glutathione level and decreased an antioxidant activity of the superoxide dismutase and catalase.

However, in the case of rats of other groups, supplemented with N-acetyl cysteine, selenium and in combination, researchers observed protective effect against the mercury toxicity (mercury poisoning). This result revealed that a combination of N-acetyl cysteine and selenium is much more effective in protecting against poisoning caused by mercuric chloride by preventing oxidative damage of biological membranes from free radical attacks mediated by the mercury poisoning.

Reference: Journal of Trace Elements in Medicine and Biology Article doi:10.1016/j.jtemb.2013.12.006

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