Hannaneh Wahhabaghai

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OBJECTIVE Exposure to normobaric hyperoxia protects the heart against ischemia-reperfusion injury ex vivo. In the present study, we investigated the effect of the early and late phase of hyperoxia on in vivo myocardial infarction and apoptosis. METHODS Rats were exposed to room air preoxygenation (O(2)≥ 95%) followed by regional ischemia (30 min) and 0,(More)
BACKGROUND Pre-exposure to hyperoxic gas (>or= 95%) has been shown to protect the heart and central nervous system from ischemia-reperfusion injury. In the present study, we investigated whether oxygen pretreatment induces delayed renal protection in rats. The possible role of some renal antioxidant agents was also investigated. MATERIALS AND METHODS(More)
Cisplatin (CP) nephrotoxicity is mainly due to reactive oxygen species. Oxygen pre-exposure as a mild oxidative stress may enhance some endogenous defense mechanisms, so its effect on cisplatin-induced acute renal failure was investigated in present study. Twenty-four rats were divided into four groups. The O(2)+ CP and Air + CP groups were were subjected(More)
BACKGROUND Renal injury is the main side effect of cisplatin (CP), an anticancer drug. It has been shown that pretreatment with single-dose oxygen (0.5 to six hours) could reduce CP-induced renal toxicity in rats. OBJECTIVES The present study aimed to compare the effects of pretreatment with single-dose and intermittent O2 on CP-induced nephrotoxicity. (More)
Late respiratory complications in patients suffering from pulmonary lesions due to sulfur mustard (SM) gas are asthma, chronic obstructive pulmonary disease and bronchiectasis. Recently PON1 antioxidant activity draws attention as the enzyme which prevents the oxidation of lipoproteins during oxidative stress. In this study we aimed to investigate PON1 192(More)
OBJECTIVE Pre-exposure of rats to normobaric hyperoxia (O2 ≥ 95%) may induce late preconditioning against renal ischemia-reperfusion (IR) injury. In this study we investigated probable mechanisms of IR injury such as the role of reactive oxygen species (ROS), renal antioxidant agents, and heat shock proteins (HSP) 32 and 70 during delayed(More)
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