Antioxidants

Abstract

Over the past several years, advances in our understanding of the pathogenesis of acute kidney injury (AKI) have demonstrated the role of oxidant stress and reactive oxygen metabolites (ROM) in the development of AKI in a variety of clinical settings. This review serves to define the pathways that lead to the generation of ROM following a variety of insults, as well as to review the current literature concerning the role of antioxidant therapy in the prevention and treatment of AKI in several clinical settings. Investigators have explored the potential therapeutic role of anti-oxidants in both experimental animal models and human studies of AKI in several clinical settings, including cardiac and aortic occlusive surgeries, sepsis, drug nephrotoxicity (cisplatin and gentamicin), as well as rhabdomyolysis. While the experimental animal studies have generally been more successful, taken together this literature supports the hypothesis that oxidant stress-induced production of ROM plays a major role in the pathogenesis of many forms of AKI, and continues to suggest the potential utility of antioxidant therapy in human AKI. Ongoing trials in concert with improved diagnostic techniques will hopefully lead to improved outcomes in the setting of AKI through the prophylactic or early therapeutic use of antioxidant therapy.

Evaluation of the Potential Nephroprotective and Antimicrobial Effect ofCamellia sinensisLeaves versusHibiscus sabdariffa(In VivoandIn VitroStudies)

“…The basis of the protective action of those plant extracts is not known with certainty, but it was thought to be directly related to their antioxidant properties [32, 33]. In addition, Kadkhodaee et al, 2005 and Kadkhodaee et al, 2007, found that the nephroprotective effect of green tea may be due to the presence of vitamins C and E in its composition [34, 35].…”

Hypoxia-Inducible Factor Activation Protects the Kidney from Gentamicin-Induced Acute Injury

“…Oxidative stress plays an important role in the nephrotoxicity of gentamicin [27]. There have been reports that treatment with gentamicin produces oxidative stress in renal tubule cells, both in vivo and in vitro [28], [29].…”

“…There have been reports that treatment with gentamicin produces oxidative stress in renal tubule cells, both in vivo and in vitro [28], [29]. Therefore, there have been many attempts to study the effects of antioxidants on the reduction of renal dysfunction and tissue damage induced by gentamicin [6], [27], [30], [31]. However, there has been only one study of the role of antioxidants in modulating the direct cytotoxic effects of gentamicin on renal tubule cells [29].…”

Pathophysiology of Cisplatin-Induced Acute Kidney Injury

“…Sodium thiosulfate [121] and metabolites of amifostine (WR-2721) have been known for a very long time to inactivate toxic platinum species and protect against cisplatin nephrotoxicity [122]. Amifostine decreases nephrotoxicity probably by donating antioxidant thiol groups [123, 124]. Hydroxyl radical scavengers such as dimethyl sulfoxide (DMSO), mannitol, and benzoic acid significantly reduced cisplatin-induced cytotoxicity.…”