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  • Our data indicate that curcumin reduced MDA and


    Our data indicate that curcumin reduced MDA and LOOH formation in plasma and kidney induced by gentamicin treatment. The results demonstrate the protective effect of this compound against oxidative damage to these membranes. Moreover, the ability of curcumin to reduce the formation of LOOH induced by exogenous oxidants (1mM FeSO4, 1mM ascorbate, 0.2mM H2O2) ex vivo underscores the potential value of this compound as a renoprotective agent. However, curcumin was unable to attenuate gentamicin-induced formation of LOOH in the presence of exogenous oxidants both in the plasma and kidney indicating the limitation of the compound as an antioxidant in the face of overwhelming ROS.
    Materials and methods
    Result The data from various groups for the individual parameters are presented as bar diagram and table with mean±STD. The present study showed that daily oral administration of 75mg/kg of aspartame for 90days led to alterations in the antioxidant status of brain, histological changes in liver and renal structures.
    Discussion Aspartame represents 62% of the value of the intense sweetener market in terms of its world consumption [40]. Upon ingestion, aspartame is immediately absorbed from the intestinal lumen and metabolized to phenyalanine, aspartic acid and methanol [41], thereby, increasing aspartame metabolites content in blood [42]. The brompheniramine maleate metabolism sequence of methanol–formaldehyde–formic acid results in synergistic damage [43]. Methanol is being increasingly recognized as a substance that damages the liver cells where it is oxidized to formaldehyde and latter to formate [13]. This study shows elevated blood formate level in aspartame treated MTX animals. However, MTX treated animals did not differ much from the control group. The accumulation of formate rather than methanol is itself considered to cause methanol toxicity [44]. A significant loss in body weight was observed in methanol-exposed rats [45]. Similarly, a decrease in the body weight, brain and liver weight was observed in aspartame treated MTX. In our earlier report for the same dose of aspartame, an increase in blood methanol during its metabolism was observed [18]. This is supported by study carried out by [12] significantly increases in small amount of aspartame in plasma methanol level. Moreover, this increase in blood methanol level was associated with a marked increase in the free radical generation in brain regions of aspartame treated MTX animals [18]. Skrzydlewska et al. [46] showed that rats intoxicated with methanol had multiple impairment of antioxidant potential in the brain. This may indicate the role of methanol metabolism outside the liver. It is relevant to point out that in the earlier report on aspartame, there was marked increase in the corticosteroid level in the plasma for the same dose [18], which indicates that the dietary sweetener aspartame could act as a chemical stressor activating the HPA axis. Free radicals formed during the methanol oxidation can also cause formation of protein peroxides. These changes may result in denaturation, aggregation and fragmentation of proteins, altering physicochemical properties and potentially losing of enzymatic activities [47]. This calls for the investigation of the involvement of antioxidant enzymes and non-enzymatic antioxidants in methanol intoxication induce oxidative stress. The antioxidant potential involving cellular GSH content and the activities of related enzymes were decreased in liver during methanol intoxication [48]. Depletion of cellular GSH increases cell vulnerability to oxidative stress [49]. This can be well correlated with increase in free radical and this may be the reason behind the decrease in the activity of liver GSH, as well as decrease in brain GR activity in aspartame treated MTX animals. The decrease in GSH activity observed in the present study seems to have been caused by methanol, because methanol metabolism depends upon GSH [18], [50], which reported similar decrease GSH level in brain for the same dose lending support to the present findings. GR plays an important role in cellular antioxidant protection by catalyzing the reduction of GSSG to GSH [51]. A decrease in glutathione levels reduces formaldehyde metabolism, thereby, increasing its toxicity, attributing to the unavailability of GSH. This decrease in GSH may be due to the rapid reaction of GSH with formaldehyde to form nucleophilic adducts [52].