2006
DOI: 10.1016/j.ejphar.2006.01.007
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Enzymatic studies of cisplatin induced oxidative stress in hepatic tissue of rats

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Cited by 145 publications
(104 citation statements)
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“…Therefore, the depletion of GSH is an early and necessary event occurring during cisplatin-induced lipid peroxidation and subsequent toxicity. It has been suggested that the levels of GSH in the liver are significantly reduced by cisplatin treatment, although very little information is currently available regarding cisplatin-induced liver injury and the mechanisms underlying its hepatotoxicity (42,43), and this suggestion was corroborated in our repeated preliminary experiments (data not shown). In the present study, our results showed that the repeated oral administration of ISL in combination with cisplatin treatment prevented cisplatin-mediated increases in the levels of serum nitric oxide and tissue lipid peroxidation, and also recovered the depleted GSH levels in tissue to a significant degree.…”
Section: Discussionsupporting
confidence: 76%
“…Therefore, the depletion of GSH is an early and necessary event occurring during cisplatin-induced lipid peroxidation and subsequent toxicity. It has been suggested that the levels of GSH in the liver are significantly reduced by cisplatin treatment, although very little information is currently available regarding cisplatin-induced liver injury and the mechanisms underlying its hepatotoxicity (42,43), and this suggestion was corroborated in our repeated preliminary experiments (data not shown). In the present study, our results showed that the repeated oral administration of ISL in combination with cisplatin treatment prevented cisplatin-mediated increases in the levels of serum nitric oxide and tissue lipid peroxidation, and also recovered the depleted GSH levels in tissue to a significant degree.…”
Section: Discussionsupporting
confidence: 76%
“…It has been proposed that oxidative stress exists in the early stage of cisplatin-induced nephrotoxicity and also in hepatotoxicity (Iraz et al, 2006;Mansour et al, 2006;Pratibha et al, 2006;Satoh et al, 2000). In rats, mitochondrial dysfunction in kidney and liver was evidenced after cisplatin treatment.…”
Section: Cellular Response To Cisplatin and Oxidative Stressmentioning
confidence: 95%
“…Cisplatin in the present study produced significant reduction of the activities of plasma catalase (an antioxidant enzyme), plasma total antioxidant capacity accompanied by increased lipid peroxidation compared with the control rats. The renal oxidative stress may have resulted from the build-up of ROS such as O 2 -and H 2 O 2 following the decrease in the activities of the renal antioxidant enzymes, which is typical during cisplatin treatment [Pratibha et al, 2006]. The increased generation of O 2 -and H 2 O 2 leads to increased production of the more reactive hydroxyl (OH -) radical via Fenton and Haber-Weiss reactions [Stadtman, 1990].…”
Section: Discussionmentioning
confidence: 99%