Nevertheless, considering the reports on the impact of CTX on malaria, both in HIV-infected and uninfected individuals, we reviewed the available evidence on safety and efficacy of CTX as an antimalarial for both preventive and curative use. It has been well established that exposure to heavy metals including a number of environmental pollutants can cause cellular damages through the formation of highly reactive substances such as reactive oxygen species. ROS show a wide range of pathophysiology. The present study established that exposure to lead nitrate Pb significantly increased ROS formation, enhanced oxidative stress and induced apoptosis in the liver tissue of experimental mice. This adverse effect of Pb, however, could be eliminated by mangiferin treatment probably because of its strong free radical scavenging activity. Besides dietary antioxidants, the body depends on several endogenous defense mechanisms to protect against ROS-induced cell damage. Among these antioxidant molecules, SOD and CAT jointly play important roles in the Orbifloxacin exclusion of ROS. With the purpose of removing excess free radicals from the system, GST and GPx use GSH in their course of reactions. Diminish in GSH content because of oxidative stress reduce the actions of GST and GPx with a concomitant 4-(Benzyloxy)phenol decrease in the activity of GSH stimulating enzyme, GR. The sulfhydryl group of GSH directly binds to heavy metals due to a high affinity for sulfhydryl groups. Lead, arsenic and mercury effectively inactivate the glutathione molecule so it is unavailable as an antioxidant or as a substrate in liver metabolism. In the present study, we found that Pb exposure decreased the activities of the antioxidant enzymes, CAT, SOD, GST, GPX and GR in addition to the level of GSH in the liver tissue. Pbintoxication is also connected to the increased hepatic levels of lipid peroxidation and protein carbonylation and serum marker enzymes. But post treatment of animals with mangiferin after Pb exposure could change the alterations in the activities of the antioxidant enzymes and the level of GSH. It also modulated the levels of lipid peroxidation and protein carbonylation and serum marker enzymes. We studied Pb induced mode of cell death and its protection by mangiferin using DNA fragmentation and flowcytometric analyses. DNA fragmentation is one of the most often used techniques in the study of cell death. Internucleosomal DNA fragmentation can be visualized by gel electrophoresis as 
the characteristic DNA ladder formation and was considered as a biochemical hallmark of apoptosis. In our study, DNA gel electrophoresis showed that Pb exposure caused DNA fragmentation which appeared as a ladder in the agarose-ethidium bromide gel. The result of this study clearly suggests that Pb induced cell death occurred via apoptotic pathway. Mangiferin could, however, inhibit the Pb induced DNA fragmentation and apoptotic cell death. Flowcytometric analyses also demonstrated that Pb mostly damaged hepatocytes via apoptotic pathway. Simultaneous treatment with mangiferin, on the other hand, decreased the degree of Pbinduced apoptotic cell death. Multicellular organisms have three well-characterized subfamilies of mitogen activated protein kinases. The members of the family are basically serine/ threonine kinases, activated by dual phosphorylation on their threonine and tyrosine residues and are projected as critical redox signaling proteins.