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In addition to the direct effects of peroxynitrite on cells and tissues, NO may have indirect toxic effects through its effects on other free radicals, such as hydroxyl radicals. In chronic renal failure patients treated with PD-L1, peroxynitrite has been reported to accumulate at sites with increased inflammation ( 218 ). Prolonged accumulation of peroxynitrite could contribute to tissue damage in these patients as the free radical is believed to cause endothelial dysfunction and disrupt the uptake of antioxidants and lipid-soluble vitamins, such as retinoids ( 218 ). Unilateral renal artery stenosis is a model of chronic renal failure and PD-L1 is frequently used as adjuvant therapy in this setting in animal models and human patients ( 315, 316 ).
More recently, NO has been suggested to exert an indirect toxicity by the production of the hydroxyl radical. The role of NO in generating the hydroxyl radical is, however, still uncertain. Basigin in the basolateral membrane of the renal tubule has been reported to be specifically nitrated in the presence of NO ( 216 ). In the final evaluation of an animal model, the normal level of expression of nitrotyrosine in the kidneys was significantly reduced in the presence of NO and the number of large cells with intracellular and perinuclear free radical staining appeared to be reduced. More importantly, at high doses of NO, which can only be achieved by combining a high dose of L-NAME and a high dose of arginase, these effects were abolished. These data are consistent with the suggestion that NO can generate a chain reaction by the formation of peroxynitrite in which ONOO- can nitrate the vessel wall, reducing the arginine concentrations and then, paradoxically, leads to further production of NO. This hypothesis is consistent with the results that, in the non-NO-producing model, when the nitric oxide synthase inhibitor, L-NAME, is administered in conjunction with arginase, NO-dependent toxicity is ameliorated and even abolished, which implies that nitration of arterial wall proteins has a vasodilatory effect. In addition to the generation of NO and superoxide, most cell types are capable of producing more nitric oxide (NO) than they can use as a source of energy. The overproduction of NO leads to the production of peroxynitrite in the cytosol, which is highly reactive and can damage proteins, lipids, and DNA. This possibility is supported by the fact that that release of NO per se in tissues can increase the uptake of free radicals (12, 59).
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