Hyperoxia induced protection against rat's renal ischemic damage: Relation to oxygen exposure time

Cisplatin toxicity reduced in human cultured renal tubular cells by oxygen pretreatment

“…6,12,13 The present study demonstrates that this beneficial effect of oxygen pretreatment also is present in human renal tubular cells. Previously proposed mechanisms which could also explain somewhat the present study findings, is that sub-lethal excess amount of free radicals produced during oxygen pretreatment 29 may act as a mediator for induction of cellular protective agents like antioxidant enzymes, 13 heat shock proteins (Wahhabaghai et al, unpublished data) and probably other endogenous defense mechanisms. Figure 4.…”

“…3,11 Previous animal studies have shown that short-term pretreatment with nearly pure oxygenwithout closing to the oxygen toxicity threshold-could lead to some degrees of protection against Cisplatin induced nephrotoxicity and both renal and cardiac ischemic damages. 6,[12][13][14][15] This protective effect may be due to stimulating the endogenous defense mechanisms such as antioxidant systems against free radicals by mild hyperoxia-induced oxidative stress.…”

Pretreatment with hyperoxia reduces in vivo infarct size and cell death by apoptosis with an early and delayed phase of protection

“…Several studies have shown that exposure to short periods of hyperoxia evokes protection against ischemia in the heart [2][3][4][7][8][9], kidney [6], and brain [5]. Prolonged exposure to a hyperoxic environment (more than 12-24 h) can lead to injury of different organs [5].…”

“…Previous investigations in animal models show that short exposure to normobaric hyperoxia mimics preconditioning and protects the isolated heart against ischemic injury and reperfusion-induced arrhythmias in a biphasic mode analogous to early and delayed protection by ischemic preconditioning [2][3][4]. Pretreatment with normobaric hyperoxia also protects the brain and kidney [5,6] against subsequent ischemia-reperfusion injury. Recently, we performed a dose-response study on hyperoxic pretreatment on in vivo myocardial infarction, and found that preexposure to 120 and 180 min normobaric hyperoxia was most protective, reducing infarct size and the incidence of ventricular fibrillation [7].…”