The role of nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR-γ) and Nrf2 signalling in methanol-induced on brain, eye, and pancreas toxicity in rats.

Toxic methyl alcohol is widely employed in industry, and it is highly toxic. Only 15 cc ingestion can result in irreversible blindness. The mechanism of toxicity is still a matter of debate. This study was conducted to investigate the incorporation of nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR-γ) and Nrf2 signaling pathways in the toxicity of the brain, eye, and pancreas following ingestion of methyl alcohol and the possible protective role of PPAR-γ modulators. Twenty-four adult Wister albino rats were divided into four groups of six rats each: a control group, a pioglitazone group, a methanol group, and a combined pioglitazone and methanol group. Oxidative stress markers, random blood sugar, insulin, and pancreatic function measurements were evaluated. Western blot analysis for PPAR-γ and Nrf2 protein expressions was performed. Histopathological examination was performed for eye, brain, and pancreas tissues, and the results were compared. PPAR-γ seemed to be incorporated in the development of organ toxicity associated with methyl alcohol ingestion. The protective role of PPAR-γ modulators was achieved through the improvement of assessed pathways. Therefore, damage can be dramatically improved through incorporating PPAR-γ agonists in the management plan of methyl alcohol toxicity.