Protective effect of dl-α-lipoic acid on cyclophosphamide induced oxidative cardiac injury

Mythili, Yenjerla; Sudharsan, Periyasamy Thandavan; Selvakumar, E.; Varalakshmi, P.

doi:10.1016/j.cbi.2004.10.004

Cited by 95 publications

(70 citation statements)

References 31 publications

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“…119 Although a precise mechanism of cardiac injury has not been elucidated, preclinical studies suggest that the active phosphoramide mustard causes increased free radical formation in cardiac tissue, leading to cell damage. 120 Autopsies of patients who suffered fatal cyclophosphamide-induced HF indicate the presence of hemorrhagic myocarditis. The presence of microthrombi and proteinaceous exudates suggests significant endothelial damage with cyclophosphamide.…”

mentioning

confidence: 99%

Drugs That May Cause or Exacerbate Heart Failure

Page¹,

O’Bryant²,

Cheng³

et al. 2016

Circulation

348

185

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Heart failure is a common, costly, and debilitating syndrome that is associated with a highly complex drug regimen, a large number of comorbidities, and a large and often disparate number of healthcare providers. All of these factors conspire to increase the risk of heart failure exacerbation by direct myocardial toxicity, drug-drug interactions, or both. This scientific statement is designed to serve as a comprehensive and accessible source of drugs that may cause or exacerbate heart failure to assist healthcare providers in improving the quality of care for these patients.

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mentioning

confidence: 99%

Drugs That May Cause or Exacerbate Heart Failure

Page¹,

O’Bryant²,

Cheng³

et al. 2016

Circulation

348

185

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“…Motawi et al (2010) found that at higher doses of CP (200 mg/kg), there was heart damage as a result of the high oxidative stress, NO and MDA and decreased GSH and TAS levels. In some clinic and experimental studies (Mythili et al 2004;Fatani et al 2010), it has been observed that high doses of CP increased the serum levels of CK-MB, LDH, ALT and AST. Zarei and Shivanandappa (2013) reported that the serum levels of ALT, AST, LDH, SOR and lipid peroxidation levels increased and GSH, AO eynzyme activities decreased with the CP treatment in the rats.…”

Section: Resultsmentioning

confidence: 99%

Protective Effect of Carvacrol Against Oxidative Stress and Heart Injury in Cyclophosphamide-Induced Cardiotoxicity in Rat

Çetik

Ayhancı

Şahıntürk

2015

Braz. arch. biol. technol.

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“…The elevation in activities of these enzymes in serum is diagnostic marker for cardiac injury. Cisplatin has the ablility to generate reactive oxygen species, such as superoxide anion and hydroxyl radical (5), that results in irreversible modifi cation of myocardial membrane structures, functions and integrity with the consequent leakage of cardiac enzymes (13,15).…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have shown that LA exerts multiple pharmacological actions in different models of diseases characterized by increase in oxidative stress markers (9)(10)(11). Additionally, the cardioprotective effects of LA against adriamycin and cyclophosphamide induced-toxicities are well documented (12,13). Moreover, LA exerts antiinflammatory actions by inhibiting nuclear factor-κB (NF-κB) activation and by decreasing adhesion molecule expression in endothelial cells (14).…”

Section: Introductionmentioning

confidence: 99%

Ameliorating effect of DL-α-lipoic acid against cisplatin-induced nephrotoxicity and cardiotoxicity in experimental animals

Hussein¹

2012

Drug Discov Ther

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Cisplatin is a potent chemotherapeutic agent with a wide range of activities. Nephrotoxicity and cardiotoxicity represent it's major complication upon clinical use. The present study was carried out to evaluate the possible protective effect of DL-α-lipoic acid (LA) against cisplatin-induced nephrotoxicity and cardiotoxicity. Different groups of rats (n = 10) were administered either saline (control), cisplatin (10 mg/kg, i.p.), LA (100 mg/kg, i.p.) or their combination (LA 30 min prior to cisplatin administration). Twentyfour hours later all animals were decapitated and sera were used for estimation of activities of urea (BUN), creatinine (Cr), lactate dehydrogenase (LDH), and creatine kinase (CK). Homogenates of the kidney and heart were used for estimation of oxidative stress markers (reduced glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO)). Additionally, caspase-3 activities and DNA-fragmentation were investigated in renal tissues. The results showed that cisplatin produced significant elevation in serum activities of LDH, CK, BUN, and Cr and also induced significant elevation in the oxidative stress makers (MDA and NO) accompanied by significant reduction in GSH and SOD in both kidney and heart. The integrity of DNA was heavily damaged and caspase-3 was activated in renal tissues. The results emphasized nephrotoxicty and cardiotoxicity of cisplatin. On the other hand, prior administration of LA significantly attenuated the cisplatin-evoked disturbances in the above mentioned parameters and protected both kidney and heart tissues. The histopathological examination emphasized the obtained results. In conclusion, LA is suggested to be a potential candidate to ameliorate cisplatininduced nephrotoxicity and cardiotoxicity without altering the antitumor efficacy of cisplatin.

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Protective effect of dl-α-lipoic acid on cyclophosphamide induced oxidative cardiac injury

Cited by 95 publications

References 31 publications

Drugs That May Cause or Exacerbate Heart Failure

Drugs That May Cause or Exacerbate Heart Failure

Protective Effect of Carvacrol Against Oxidative Stress and Heart Injury in Cyclophosphamide-Induced Cardiotoxicity in Rat

Ameliorating effect of DL-α-lipoic acid against cisplatin-induced nephrotoxicity and cardiotoxicity in experimental animals

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