Effect of dl-α-lipoic acid on cyclophosphamide induced lysosomal changes in oxidative cardiotoxicity

Mythili, Yenjerla; Sudharsan, Periyasamy Thandavan; Amudha, Ganapathy; Varalakshmi, P.

doi:10.1016/j.lfs.2007.02.040

Cited by 17 publications

(5 citation statements)

References 37 publications

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“…Data presented here demonstrated that CP increased serum cardiotoxicity enzymatic indices, LDH, and CK-MB. These results are consistent with the data presented by several authors [12,16,[40][41][42], who demonstrated a marked elevation of CK-MB, LDH, ALT, and AST, 10 days after administration of a single dose of CP (200 mg/kg). This increase in cardiotoxicity enzymatic indices could be explained on the basis of CPinduced lipid peroxidation of cardiac membranes with the consequent leakage of cardiac enzymes from damaged cardiac myocytes to the serum.…”

Section: Discussionsupporting

confidence: 93%

Thymoquinone supplementation attenuates cyclophosphamide‐induced cardiotoxicity in rats

Nagi

Al‐Shabanah

Hafez

et al. 2010

J Biochem & Molecular Tox

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This study examined the possible protective effects of thymoquinone (TQ), the main constituent of the volatile oil of black seed (Nigella sativa), against cyclophosphamide (CP)-induced cardiotoxicity. Adult male Wistar albino rats were divided into four treatment groups. Rats in the first group were served as control. Rats in the second group received TQ (50 mg/L in drinking water) for 12 days. Animals in the third group were injected with a single dose of CP (200 mg/kg, IP) at day 5. Rats in the fourth group received TQ (50 mg/L in drinking water) for 5 days before a single dose of CP (200 mg/kg, IP) and continued thereafter throughout the experiment. On day 13, animals were sacrificed; serum and hearts were isolated and analyzed. Cyclophosphamide resulted in a significant increase in serum creatine kinase, lactate dehydrogenase, cholesterol, triglycerides, creatinine, urea, and tumor necrosis factor-α. In heart tissues, CP resulted in a significant increase in thiobarbituric acid reactive substances and total nitrate/nitrite and a significant decrease in reduced glutathione, glutathione peroxidase, catalase, and adenosine triphosphate levels. Interestingly, TQ supplementation resulted in a complete reversal of all the biochemical changes induced by CP to their control values. Data from this study suggest that TQ supplementation attenuates CP-induced cardiotoxicity by a mechanism related, at least in part, to its ability to decrease oxidative and nitrosative stress and to preserve the activity of antioxidant enzymes as well as its ability to improve the mitochondrial function and energy production. .

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Section: Discussionsupporting

confidence: 93%

Thymoquinone supplementation attenuates cyclophosphamide‐induced cardiotoxicity in rats

Nagi

Al‐Shabanah

Hafez

et al. 2010

J Biochem & Molecular Tox

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“…These results are in agreement with previous reports of increased production of ROS and depletion of the mitochondrial antioxidant defence system in kidney, heart, brain, liver, testis and urinary bladder . The free radicals are generated in vivo by various mechanisms, including mitochondrial dysfunction, respiratory burst and the activity of various oxidases . The possible mechanism for the free radical‐induced mitochondrial dysfunction appears to be the inactivation of respiratory‐chain enzymes, such as NADH‐cytochrome c reductase and succinate‐cytochrome c reductase, by the induction of metal‐catalysed oxidation within the active centres of the respiratory‐chain complexes.…”

Section: Discussionsupporting

confidence: 91%

Crocin, a dietary colorant mitigates cyclophosphamide-induced organ toxicity by modulating antioxidant status and inflammatory cytokines

Jnaneshwari

Hemshekhar

Santhosh

et al. 2013

Journal of Pharmacy and Pharmacology

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“…Mythili et al [77] Male Wistar albino rats Rats received CP (200 mg/kg i.p. ), which is immediately followed by lipoic acid (25 mg/kg orally) for 10 days.…”

Section: Oxidative Medicine and Cellular Longevitymentioning

confidence: 99%

The Role of Antioxidants in Ameliorating Cyclophosphamide-Induced Cardiotoxicity

Ayza

Zewdie

Tesfaye

et al. 2020

Oxidative Medicine and Cellular Longevity

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The chemotherapeutic and immunosuppressive agent cyclophosphamide has previously been shown to induce complications within the setting of bone marrow transplantation. More recently, cardiotoxicity has been shown to be a dose-limiting factor during cyclophosphamide therapy, and cardiooncology is getting wider attention. Though mechanism of cyclophosphamide-induced cardiotoxicity is not completely understood, it is thought to encompass oxidative and nitrative stress. As such, this review focuses on antioxidants and their role in preventing or ameliorating cyclophosphamide-induced cardiotoxicity. It will give special emphasis to the cardioprotective effects of natural, plant-derived antioxidants that have garnered significant interest in recent times.

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Effect of dl-α-lipoic acid on cyclophosphamide induced lysosomal changes in oxidative cardiotoxicity

Cited by 17 publications

References 37 publications

Thymoquinone supplementation attenuates cyclophosphamide‐induced cardiotoxicity in rats

Thymoquinone supplementation attenuates cyclophosphamide‐induced cardiotoxicity in rats

Crocin, a dietary colorant mitigates cyclophosphamide-induced organ toxicity by modulating antioxidant status and inflammatory cytokines

The Role of Antioxidants in Ameliorating Cyclophosphamide-Induced Cardiotoxicity

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