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A 400 mg/kg dose provided protection that was substantial [13]

Pharmacological inhibition of mitochondrial carbonic anhydrases protects mouse cerebral pericytes from high glucose-induced oxidative stress and apoptosis

13 males) in the HC group

The possibility of minimizing iron intake or removing iron may prove beneficial for the treatment of liver injury and it is clearly an area that deserves further research ( For investigating the pathogenesis and treatment of APAP-induced hepatotoxicity, the role of iron was evaluated as was whether PA played a role in the treatment of APAP-induced hepatotoxicity in light of its importance as an iron chelator and its ability to block the generation of iron-driven hydroxyl radicals as well as the suppression of lipid peroxidation ( The serum iron could reflect hepatic iron accumulation, which is considered an important factor in the progression of liver fibrosis ( On exposure to a toxic dose of APAP, ferrous iron is released into the cytosol from the ruptured lysosomes ( The current results showed that APAP treatment induced a statistically significant increase in MDA and a decrease in GSH levels compared to the control group, while PA produced a significant improvement in oxidative stress by decreasing the MDA level and increasing the GSH level compared to the APAP group