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The possible function of nitric oxide (NO) in iron-induced toxicity was investigated in proximal tubule cells in primary culture. Findings showed that NO production and NO synthase activity heightened in culture promixal cells by iron treatment. Therefore, NO is one of the mediators of iron-induced toxicity in proximal tubule cells. Toxicity caused by NO is not affected by lipid peroxidation.

Reactive iron released from lysosomes causes peroxidative damage to the cytoplasm in patients who have lost part of a kidney due to surgery. Endocytosis across the proximal tubule luminal membrane absorbs filtered transferrin iron into lysosomes. Lysosomal destabilization or reactive oxygen species generation may cause proximal tubule (PT) injury when there is iron accumulation in PT, in humans and animals with chronic renal disease. A study is conducted on remnant kidney and sham-operated Wistar rats.