Arsenic aggravates oxidative stress causing hepatic alterations and inflammation in diabetic rats

Studies have shown that exposure to either environmental toxicants or hyperglycemia causes hepatic injuries. However, it is unclear the extent to which their combined exposure may influence liver functions. Therefore, we aimed to evaluate morphological and functional hepatic parameters in diabetic rats exposed to arsenic.

Diabetes was induced in male rats by intraperitoneal streptozotocin injection. While healthy and diabetic animals received saline solution (negative control and diabetes control, respectively), other animals received 10 mg/L sodium arsenate (arsenic control and diabetes + arsenic groups, respectively) for 40 days in drinking water. Liver tissue was subjected to antioxidant enzymes analysis, cytokine assay, arsenic determination, and histopathological evaluation. Functional markers of hepatic damage were analyzed using serum samples.

Arsenate exposure reduced the antioxidant enzymes activity in healthy rats, and it worsened the reduction of GST in diabetic animals. Consequently, arsenate-exposed animals showed increased malondialdehyde and carbonyl protein levels, being this increase worsened in diabetes + arsenic animals. Arsenate-exposed groups also showed hepatic inflammatory process with high number of mast cells and TNF-α production mainly in diabetes + arsenic animals. Vascular alterations, such as congestion, bleeding, and hemosiderin deposition were intensified in diabetes + arsenic animals, whereas glycogen storage reduced in these animals.

We concluded that arsenate exposure was able to intensify morphological and functional damages in liver tissue of diabetic animals.