Oxidative stress has been identified as the root cause of the development and progression of several diseases. Supplementation of exogenous antioxidants or boosting endogenous antioxidant defenses of the body is a promising way of combating the undesirable effects of reactive oxygen species (ROS) induced oxidative damage. Plants have an innate ability to biosynthesize a wide range of non-enzymatic antioxidants capable of attenuating ROS- induced oxidative damage. Several in vitro methods have been used to screen plants for their antioxidant potential, and in most of these assays they revealed potent antioxidant activity. However, prior to confirming their in vivo therapeutic efficacy, plant antioxidants have to pass through several physiopharmacological processes. Consequently, the findings of in vitro and in vivo antioxidant potential assessment studies are not always the same. Nevertheless, the results of in vitro assays have been irrelevantly extrapolated to the therapeutic application of plant antioxidants without undertaking sufficient in vivo studies. Therefore, we have briefly reviewed the physiology and redox biology of both plants and humans to improve our understanding of plant antioxidants as therapeutic entities. The applications and limitations of antioxidant activity measurement assays were also highlighted to identify the precise path to be followed for future research in the area of plant antioxidants.
Taken together, the results suggest that kidney is the major target tissue to suffer impairment of mitochondrial function with the onset of the disease which persists throughout and that insulin treatment is ineffective in restoring the normal state.
Long-term exposure to AlCl3 resulted in 57% decrease in the total phospholipid (TPL) content of synaptic plasma membranes from rat brain with significant decrease in the proportion and content of most of the phospholipid classes (32%-77% decrease); the extent of decreases was of lesser magnitude for phosphatidylcholine (PC) and phosphatidylethanolamine (PE). The microsomal TPL and cholesterol (CHL) content decreased by 74% and 35% with marginal changes in the phospholipid composition. However, the contents of all phospholipids decreased uniformly by about 70%. The synaptic plasma membranes were more fluidized in Al fed rats. The results suggest that long-term exposure of rats to Al can alter the structure/function of synaptic plasma membranes and microsomes.
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