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Dietary aluminum exposure induces several biochemical and histopathological alterations in experimental animals. Since endothelial dysfunction is one of the earliest signs of disseminated intravascular coagulation (DIC), this study was designed to evaluate the beneficial effect of Al on endothelial dysfunction in a rat model of DIC. The rats were given Al in a high-fat diet for eight weeks. Platelet count, fibrinogen level, and the prothrombin time were monitored at regular intervals. The levels of malondialdehyde, reduced glutathione, and pro-inflammatory cytokine TNF-alpha were also measured. The protein expression of inducible nitric oxide synthase (iNOS) was studied using western blot analysis. In vitro assays were also done to investigate the effect of Al on NO production and barrier functions of bovine endothelial cells. In vivo study showed Al to have a beneficial effect on DIC by increasing platelet count and prolonging the prothrombin time. Furthermore, Al treatment normalized oxidative stress, increased the thiols levels and decreased malondialdehyde in plasma. The protein expression of iNOS and the levels of TNF-alpha were lowered significantly in Al-treated animals. In vitro study showed Al treatment to decrease the levels of nitrite in the culture supernatant and to increase the levels of 0b46394aab
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