Investigating the effects of dihydroxyacetone on oxidative stress factors and histology of heart and liver tissue in acute aluminum phosphide poisoning

Aluminum phosphide poisoning has a high mortality rate because of the production of phosphine gas and refractory hypotension. Based on the effect of dihydroxyacetone on the treatment of hypotension and reduction of cytochrome C oxidase, the effects of dihydroxyacetone on the level of oxidative stress factors and histology of heart and liver tissue in aluminum phosphide-poisoned male rats were investigated.

In this study, 24 rats were randomly divided into 4 groups including control (corn oil), aluminum phosphide (15 mg/kg), dihydroxyacetone (50 mg/kg) and also poisoned and treated group (aluminum phosphide (15 mg/kg) + dihydroxyacetone (50 mg/kg)). After 24 hours, the animals were sacrificed and the blood, plasma, heart, and liver samples were collected then oxidative stress factors and histology of the heart and liver were investigated.

Aluminum phosphide poisoning increased lipid peroxidation in red blood cells (p=0.001) and liver tissue (p=0.023) and also increased protein carbonylation in plasma (p =0.005) and red blood cells (p=0.001). After administration of dihydroxyacetone, lipid peroxidation in red blood cells (p=0.001) and liver (p=0.001) and carbonylation of proteins in red blood cells (p=0.003) and plasma (p=0.019) decreased. No significant change was observed in total plasma antioxidant capacity, carbonylation levels of the liver and heart, and lipid peroxidation in heart tissue. In addition, treatment with dihydroxyacetone significantly improved the histological changes in liver and heart tissue.

Dihydroxyacetone not only prevents phosphine-induced deaths but also improves oxidative stress and histology of liver and heart tissue.