Effects of the anticancer dehydrotarplatin on cytochrome P450 and antioxidant enzymes in male rat tissues

Nannelli, Annalisa; Messina, Andréa; Marini, Sandra; Trasciatti, Silvia; Longo, Vincenzo; Gervasi, Pier Giovanni

doi:10.1007/s00204-007-0184-7

Cited by 9 publications

(4 citation statements)

References 37 publications

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“…The significant reduction in GSH levels promoted by CP represents an alteration in the cellular redox state, suggesting that the cells could be more sensitive to ROS. This leads to a reduction in effectiveness of the antioxidant enzyme defense system [28]. In this study, GSH levels in the kidney tissues of rats treated with CP were lower (28%) than the control groups (p<0.05).…”

Section: Discussionmentioning

confidence: 48%

Seleno l-Methionine Acts on Cyclophosphamide-Induced Kidney Toxicity

Ayhancı

Güneş

Şahıntürk

et al. 2009

Biol Trace Elem Res

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The anticancer drug cyclophosphamide (CP) has nephrotoxic effects besides its urotoxicity, which both in turn limit its clinical utility. The nephrotoxicity of CP is less common compared to its urotoxicity, and not much importance has been given for the study of mechanism of CP-induced nephrotoxicity so far. Overproduction of reactive oxygen species (ROS) during inflammation is one of the reasons of the kidney injury. Selenoproteins play crucial roles in regulating ROS and redox status in nearly all tissues; therefore, in this study, the nephrotoxicity of CP and the possible protective effects of seleno L-methionine (SLM) on rat kidneys were investigated. Forty-two Sprague-Dawley rats were equally divided into six groups of seven rats each. The control group received saline, and other rats were injected with CP (100 mg/kg), SLM (0.5 or 1 mg/kg), or CP+ SLM intraperitoneally. Malondialdehyde (MDA) and glutathione (GSH) levels in kidney homogenates of rats were measured, and kidney tissues were examined under the microscope. CP-treated rats showed a depletion of renal GSH levels (28% of control), while CP+SLM-injected rats had GSH values close to the control group. MDA levels increased 36% of control following CP administration, which were significantly decreased after SLM treatment. Furthermore, these biochemical results were supported by microscopical observations. In conclusion, the present study not only points to the therapeutic potential of SLM in CP-induced kidney toxicity but also indicates a significant role for ROS and their relation to kidney dysfunction.

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Section: Discussionmentioning

confidence: 48%

Seleno l-Methionine Acts on Cyclophosphamide-Induced Kidney Toxicity

Ayhancı

Güneş

Şahıntürk

et al. 2009

Biol Trace Elem Res

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“…The significant reduction in GSH levels promoted by CDDP represents an alteration in the cellular redox state, suggesting that the cells could be more sensitive to ROS. This leads to a reduction in effectiveness of the antioxidant enzyme defense system [40]. In this study, GSH levels in the liver and kidney tissues of rats treated with CDDP were lower than the control group's.…”

Section: Discussionmentioning

confidence: 49%

Protective effect of L-carnitine against cisplatin-induced liver and kidney oxidant injury in rats

et al. 2009

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AbstractThe present study was designed to investigate the protective effects of L-carnitine (LC) on changes in the levels of lipid peroxidation and endogenous antioxidants induced by cisplatin (cis-diamminedichloroplatinum II, CDDP) in the liver and kidney tissues of rats. Twenty-four Sprague Dawley rats were equally divided into four groups of six rats each: control, cisplatin, L-carnitine, and L-carnitine plus cisplatin. The degree of protection produced by L-carnitine was evaluated by determining the level of malondialdehyde (MDA). The activity of glutathione (GSH), glutathione peroxidase (GSH-Px), glutathione S-transferase (GST), and superoxide dismutase (SOD) were estimated from liver and kidney homogenates, and the liver and kidney were histologically examined as well. L-carnitine elicited significant liver and kidney protective activity by decreasing the level of lipid peroxidation (MDA) and elevating the activity of GSH, GSHPx, GST, and SOD. Furthermore, these biochemical observations were supported by histological findings. In conclusion, the present study indicates a significant role for reactive oxygen species (ROS) and their relation to liver and kidney dysfunction, and points to the therapeutic potential of LC in CDDP-induced liver and kidney toxicity.

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“…The therapeutic strategy to prevent the renal toxicity is to decrease the production of ROS as much as possible or neutralize them as early as possible. The present results clarified that pretreatment with ozone significantly prevented CPinduced lipid peroxidation which manifested in reduced (MDA) and increased tGSH in the renal tissue which could be explained by decreasing the ROS formation through improvement in oxidant status [48,49] . Our data confirmed that ozone pretreatment significantly reduced urea and creatinine, improved renal function and demonstrated increase in SOD activity and hence, morphology and histological appearance.…”

Section: Table (1): Effect Of Ozone On Serum and Kidney Biochemical Psupporting

confidence: 58%

Pre-treatment of ozone therapy in rat model provides good prophylaxis against nephrotoxicity induced by cyclophosphamide

Badr¹

2016

BESPS

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Cyclophosphamide (CP) is a drug with a wide spectrum of clinical uses. It has a potent effect in treatment of many types of cancers. CP adverse side effects limit its therapeutic uses. Renal damage is one of the limiting side effects of CP. Recently; ozone therapy (OT) has important clinical effects in minimizing the renal injury. Thus, the aim of our study was to investigate whether ozone has potency to reduce the adverse toxic effects of cyclophosphamide in rat kidney. Methods: Forty male albino rats were divided in five groups: Control (C), cyclophosphamide-induced nephrotoxicity (CPIN) injected I.P. with a single dose 200mg/kg CP. Two groups treated with CP in pre-or post-treatment of ozone therapy PRO/POO; respectively and the fifth group is ozone-only treated group (OT-only), rats treated with a single I.P. dose of ozone/oxygen mixture (0.7 mg/kg). Serum and kidney tissues used to evaluate the urea and creatinine levels, histopathological examinations, oxidative stress parameters and proinflammatory cytokines expressions. Results: The results showed that CP administration caused damage in the kidney after 24 h with significant decrease in total glutathione (tGSH), super oxide dismutase (SOD) and increased in lipid peroxidation (MDA) and nitric oxide (NO) values. In line with elevations in the serum (TNF-alpha) and (IL-6). The results showed improvement in PRO group but no changes in POO group compared to the CPIN group results. Conclusions: The study represents that pre-treatment of ozone decreased the renal severity of CP in a manner leading to modulations in kidney histopathology alterations.

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Effects of the anticancer dehydrotarplatin on cytochrome P450 and antioxidant enzymes in male rat tissues

Cited by 9 publications

References 37 publications

Seleno l-Methionine Acts on Cyclophosphamide-Induced Kidney Toxicity

Seleno l-Methionine Acts on Cyclophosphamide-Induced Kidney Toxicity

Protective effect of L-carnitine against cisplatin-induced liver and kidney oxidant injury in rats

Pre-treatment of ozone therapy in rat model provides good prophylaxis against nephrotoxicity induced by cyclophosphamide

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