The potential of ADW to maintain GSH at reasonably high levels is

The potential of ADW to maintain GSH at reasonably high levels is of importance against BPA induced toxicity. Therefore,

the ability of ADW in preventing BPA induced GSH depletion by about 80% is very significant in restoring the cell viability. The GSSG formation was inhibited by ADW and this may be attributed to the formation of GSH conjugates rather than oxidation to GSSG in BPA induced toxic conditions. Earlier it was shown that Ashwagandha leaf extract and withanone, a major constituent in the leaf was beneficial to normal human fibroblasts and it showed, it was helpful to increase life span of fibroblasts by the reducing molecular damage and rendered protection against oxidative stress [41] and [42]. In yet another study, SP600125 mouse it was clearly demonstrated that withanone significantly rescued the damages caused by methoxyacetic acid mediated mitochondrial dysfunction through inhibition of excessive reactive oxygen species which were detrimental to mitochondrial function [43]. Beside these, cells secrete strong antioxidant enzymes such as superoxide dismutase, catalase and glutathione peroxidase to combat severe oxidative stress during diseased/toxic conditions. Earlier it is reported that BPA exposure results severe ROS production and results in the inhibition of antioxidant enzymes [44]. In agreement with earlier reports the antioxidant enzymes viz;

superoxide dismutase, catalase and glutathione peroxidase activities were severely diminished with addition of BPA. While addition of ADW to cells treated with BPA showed increased antioxidant enzyme activities along with increased mitochondrial AZD2281 in vivo functions. The increase in the antioxidant enzyme activities adds

to the fact that ADW restores and replenishes the antioxidant system and aids to restore normal mitochondrial functions in BPA intoxicated cells. Thus it is concluded that ADW exerts a strong cellular rejuvenation and acts as an antidote against NOAEL concentrations of BPA in HepG2 cells. Nil “
“Piroxicam, a classical NSAID, is a choice for most clinicians in arthritis and Adenosine similar clinical conditions. The possible risk of gastro-toxic effects and ulceration of gastric mucosa imposed by this drug [47] has recently restricted its use. This drug induced gastric damage is possibly caused due to oxidative stress built up in vivo in the course of its metabolism or action. Earlier studies indicated gastro-protective PGE2 synthesis leads to decreased gastro-intestinal motility, reduced blood flow and ischemia in the stomach [5].Such changes generate free hydroxyl radical (.OH) in gastric tissues. Thus, the main causative factor behind piroxicam mediated gastro-toxicity and gastric ulceration has been recognised to be .OH [8]. Leaves of the curry plant (Murraya koenigii), well known for their culinary use, have been reported to be effective in many diseased conditions [2] and [22].

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