Preventive and Therapeutic Role of Vitamin E in Chronic Plumbism

The ability of vitamin E to prevent or treat experimental lead intoxication was investigatedin rats.Lead ingestion(10 mg/kg,lead as lead acetate,orally fbr 6 weeks)significantly inhibitedthe activity of blood δ-aminolevulinic acid dehydratase(ALAD),reduced the brain dopamine(DA)contents,enhanced the blood zinc protoporphyrin,and enhanced the urinary excretion ofδ-aminolevulinic acid(ALA).Lead exposure also elevated brain norepinephrine,homovanillicacid,and 5-hydroxyindole acetic acid(5-HIAA)levels and concentration of lead in blood andtissue.Simultaneous supplementation of vitamin E along with lead significantly reduced theinhibition of blood ALAD activity,brain DA and 5-HIAA levels,and elevation of urinary ALAexcretion.Blood and liver lead concentrations were also significantly reduced by simultaneoussupplementation with vitamin E.Postlead exposure treatment with vitamin E was ineffective inreducing the lead-induced effects,except that the inhibition of blood ALAD activity was slightlyreduced.The present results suggest that vitamin E given simultaneously with lead is effectivein reducing the severity of lead intoxication.1989 Academic Press.Inc.

MiADMSA minimizes arsenic induced bone degeneration in Sprague Dawley rats

Arsenic considered as one of the most hazardous chemical while arsenic poisoning is also one of the serious medical issues worldwide.Long term arsenic exposure is associated with bone degeneration.The exact mechanism involving arsenic induced bone degeneration remains unclear but,plentiful literature suggested that oxidative/nitrosative stress caused by generation of reactive oxygen species(ROS)and reactive nitrogen species(RNS)is one of the leading causes.Various treatment strategies are available for bone degeneration however,the suitable treatment for arsenic induced bone degeneration still lacks.In the current investigation,we evaluated the efficacy of chelation against arsenic induced bone degeneration in experimental rats.Male Sprague Dawley rats were exposed to sodium arsenite and dimethylarsinic acid(DMA)(50 ppm)for 18 weeks.After arsenic exposure,animals were treated with Monoisoamyl dimercaptosuccinic acid(MiADMSA)for three course of treatment(50 mg/kg,p.o.,once daily for 5 days)with an interval of one week between two courses of treatment.MiADMSA minimizes the bone degeneration through reduction of oxidative stress(Reactive Oxygen Species,Reactive Nitrogen Species,and thiobarbituric reactive substances),alteration of antioxidant status(rGSH,Superoxide dismutase,Catalase)which led to the depletion in the levels of inflammatory markers like TNFa and IL-1b and alteration in the bone remodelling biomarkers like ALP,RANKL,and Runx2.It can be concluded from this study that MiADMSA could be an effective therapeutic strategy against arsenic induced bone degeneration and the possible mechanism could be the chelation of arsenic accompanied by the reduction in oxidative stress and inflammation.