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ABSTRACT
This study examines how Swiss albino mice's liver and kidney react to the powerful carcinogen and environmental contaminant 1,2-dimethylhydrazine (DMH). The ability of DMH to cause a range of toxicological consequences in mammalian systems is well recognized. Male Swiss albino mice were gavaged with DMH over a predetermined length of time ( 3 times a week for 2 months) to determine its hepatocellular toxicity. The liver and kidney tissues' histological, biochemical, and molecular alterations were examined. Histopathological analysis of the liver and kidney tissues indicated dose-dependent abnormalities, such as hepatocyte degradation, inflammatory cell infiltration, and glomerular changes. Significant alterations in kidney function markers (Bicarbonate which showed a value of (4.117±0.08) for the control group and DMH induced group (3.62±0.937). Urea showed a value of (0.717±0.037) for the control group and a value of (1.75±0.5) for the DMH induced group. Sodium ion showed a highly increased value in the DMH induced group (208.0±25.24) while control had a value of (114.5±5.79), potassium ion had an increase in the DMH induced group ((3.24±0.504) with the the control group value being (2.65±0.158), creatinine had a value of (2.13±0.36) for the control group and an increase in DMH induced group with value (1.88±0.2) and liver enzymes (ALT, AST) were found through biochemical examination, indicating that these organs had been damaged. This study underscores the detrimental impact of DMH exposure on the liver and kidney of Swiss albino mice and provides valuable insights into the underlying mechanisms of DMHinduced hepatorenal toxicity. Understanding these effects is crucial for developing strategies to mitigate the risks associated with exposure to this hazardous compound.