It is known that either
arsenic exposure or diabetes can impact renal function. However, it is unclear how these combined factors may influence kidney functions. Therefore, we evaluated morphological, functional, and oxidative parameters in the kidney of diabetic rats exposed to
arsenic. Healthy male Wistar rats and
streptozotocin-induced diabetic rats were exposed to 0 and 10 mg/L
arsenate through
drinking water for 40 days. Renal tissue was assessed using morphometry, mitosis and apoptosis markers,
mineral proportion, oxidative stress markers, as well as the activity of
antioxidant enzymes and membrane-bound
adenosine triphosphatases.
Arsenate intake altered
glucose levels in healthy animals, but it did not reach hyperglycemic conditions. In diabetic animals,
arsenate led to a remarkable increase of
glycogen nephrosis in distal tubules. In these animals, additionally, the activity of
catalase and
glutathione S-transferase, besides the proportion of Fe, Cu, and K in renal tissue, was altered. Nevertheless,
arsenate did not accumulate in the kidney and did not impact on other parameters previously altered by diabetes, including levels of
malondialdehyde, Na,
urea,
creatinine, and apoptosis and mitosis markers. In conclusion, besides the intensification of
glycogen nephrosis, the kidney was able to handle
arsenate toxicity at this point, preventing
arsenic deposition in the exposed groups and the impairment of renal function.