Properties of mercuric reductase from a HgCl_2-resistant fungus

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Mitochondrial dysfunction,impaired oxidative-reduction activity,degeneration, and death in human neuronal and fetal cells induced by low-level exposure to thimerosal and other metal compounds

Thimerosal (ethylmercurithiosalicylic acid), an ethylmercury (EtHg)-releasing compound (49.55% mercury (Hg)), was used in a range of medical products for more than 70 years. Of particular recent concern, routine administering of Thimerosal-containing biologics/childhood vaccines have become significant sources of Hg exposure for some fetuses/infants. This study was undertaken to investigate cellular damage among in vitro human neuronal (SH-SY-5Y neuroblastoma and 1321N1 astrocytoma) and fetal (nontransformed) model systems using cell vitality assays and microscope-based digital image capture techniques to assess potential damage induced by Thimerosal and other metal compounds (aluminum (Al) sulfate, lead (Pb)(II) acetate, methylmercury (MeHg) hydroxide, and mercury (Hg)(II) chloride) where the cation was reported to exert adverse effects on developing cells. Thimerosal-associated cellular damage was also evaluated for similarity to pathophysiological findings observed in patients diagnosed with autistic disorders (ADs). Thimerosal-induced cellular damage as evidenced by concentration- and time-dependent mitochondrial damage, reduced oxidative–reduction activity, cellular degeneration, and cell death in the in vitro human neuronal and fetal model systems studied. Thimerosal at low nanomolar (nM) concentrations induced significant cellular toxicity in human neuronal and fetal cells. Thimerosal-induced cytoxicity is similar to that observed in AD pathophysiologic studies. Thimerosal was found to be significantly more toxic than the other metal compounds examined. Future studies need to be conducted to evaluate additional mechanisms underlying Thimerosal-induced cellular damage and assess potential co-exposures to other compounds that may increase or decrease Thimerosal-mediated toxicity.     

In vitro assessment of natural plant extracts Withania somnifera,Cassia fistula,Saraca asoca,and Eucalyptus tereticornis using primary chicken embryo fibroblast cell culture treated with urea or mercuric chloride (II)

The present investigation examined the detoxifying potential of methanolic herbal extracts, namely the leaf and bark extract of Eucalyptus tereticornis, bark extract of Saraca asoca, Cassia fistula and Withania somnifera in vitro using primary chicken embryo fibroblast (CEF) cells against damaging effects of urea and mercuric chloride (HgCl) (II). The influence of 20?mM urea and 10?µM?HgCl (II) was determined on cell viability or proliferation of cells after treatment with plant extracts. Higher survival rate of primary CEF cells treated with higher concentrations of plant extracts was observed due to their protective ability against urea and HgCl (II). Cassia fistula bark extract (10?mg?mL^?1) was found to be most effective against 20?mM urea as it protects 90% of CEF cells whereas W. somnifera protects 86% of the cells within 24?h. After treating cells with10?µM HgCl, W. somnifera and E. tereticornis leaf extracts were found to be more effective among all other extracts as they protect approximately 86% and 70% of CEF cells, respectively, within 24?h. These results indicate that C. fistula and W. somnifera has the highest potential amongst all the five plant extracts for protecting CEF cells against damaging effects of urea and HgCl (II), respectively.     

Protective role of Curcuma longa extract and curcumin on mercuric chloride-induced nephrotoxicity in rats: evidence by histological architecture

Mercury (Hg) is a potent nephrotoxin. The aim of this study was to investigate the protective role of Curcuma longa extract and curcumin against HgCl₂-induced nephrotoxicity. Male Sprague Dawley rats were administered HgCl₂ (12 μmol kg^?1, ip; once only) followed by treatment of Curcuma longa extract (200 mg kg^?1, po) and curcumin (80 mg kg^?1, po) for three days after 24 h of HgCl₂ administration. The present results showed that mercuric chloride administration caused an impairment of renal function system which was evident from significant increase in urea, creatinine, uric acid, and blood urea nitrogen concentration in serum. In addition, the swelling in glomerulus and degenerated renal tubules with obstructed lumen was also observed by acute mercuric chloride administration. Treatment with Curcuma longa extract and curcumin was effective in restoring all variables of kidney functions near to control group, which was consistent with kidney histoarchitecture. In conclusion, these results suggest that Curcuma longa extract and curcumin protect against HgCl₂-induced nephrotoxicity. This study could be important for the further understanding of mercury toxicity in renal tissues and in the development of better treatments for people and/or animals exposed to the metal.