Soya milk alleviates toxicity caused by citric acid in male mice: Histopathological and hematological studies

This study evaluated the toxicity of citric acid and the benefits of soya milk (SM) for preventing damage in mice. Thirty‐five mice were divided into groups: control, mice administered citric acid (CA group) for 30 days, mice administered SM before the administration of citric acid for 30 days (SM + CA group), mice administered citric acid for 15 days and left for recovery (R group), and mice in recovery receiving SM for 15 days (R + SM). Mice in CA and R groups displayed downregulated p53, increased cleavage of caspase 3, and upregulation of Nrf2, CYP1A1, ALT, and AST activity in the liver. In contrast, SM + CA and R + SM treated mice were protected against CA toxicity and showed reversal of p53 downregulation, reduced cleavage of caspase 3, downregulation of Nrf2, and an increase in liver function enzymes. SM administration also restored blood cell and hemoglobin content and general histology of hepatocytes. Practical applications CA causes liver damage, increases inflammation, decreases blood cell numbers, and induces apoptosis. Some natural products, such as SM, have been used to scavenge free radicals that can cause liver damage and hemolysis. This study focuses on the effectiveness of SM in ameliorating CA toxicity and may be helpful in the food industry for managing oxidative stress that may be induced by common dietary constituents. SM may help suppress liver damage and inflammation. The relationship between citric acid‐induced oxidative stress, and change in the levels of P53, C‐casp.3, CYP450, NRF2 and liver function enzymes. Soya milk turnover these proteins to a normal state by regulating the level expression of P53 and it modifies the action of C.A toxicity by molecular mechanism. CA‐induced inflammation, immunopathology, apoptosis, serologic defects, and extreme hepatic damage may all be protected by soy milk.