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The protective effect of glutathione administration on adriamycin-induced acute cardiac toxicity in rats

H E Mohamed1, S E El-Swefy, H H Hagar

  • 1Department of Biochemistry, Faculty of Pharmacy, Zagazig University, Zagazig, Egypt.

Pharmacological Research
|July 11, 2000
PubMed

Insights

Glutathione (GSH) supplementation protects against Adriamycin (ADR)-induced heart damage by reducing oxidative stress. GSH depletion worsens ADR cardiotoxicity, suggesting GSH as a potential adjunct therapy for ADR treatment.

Area of Science:

  • Biochemistry
  • Cardiology
  • Pharmacology

Background:

  • Adriamycin (ADR) is an effective antitumor drug but causes significant cardiotoxicity.
  • The precise mechanisms of ADR-induced cardiotoxicity, particularly the role of free radicals, require further elucidation.
  • Glutathione (GSH), a key cellular antioxidant, plays a potential role in mitigating drug-induced organ damage.

Purpose of the Study:

  • To investigate the protective effect of glutathione (GSH) against Adriamycin (ADR)-induced cardiotoxicity in a rat model.
  • To determine the impact of GSH supplementation and depletion on biochemical and histopathological markers of cardiotoxicity.
  • To explore the potential of GSH as an adjunct therapy to limit free radical-mediated organ injury during ADR treatment.

Main Methods:

  • Male Wistar rats were administered a single dose of Adriamycin (ADR) to induce cardiotoxicity.
  • Cardiotoxicity was assessed by measuring heart rate, blood pressure, serum creatine kinase (CK), and lactate dehydrogenase (LDH).
  • Lipid peroxidation markers (MDA), homocysteine (tHcy), lipid profiles, atherogenic index, and cardiac GSH levels were analyzed. Rats were treated with GSH or depleted of GSH using L-buthionine-(S,R)-sulfoximine (BSO).

Main Results:

  • ADR administration increased heart rate, blood pressure, CK, LDH, and oxidative stress markers while decreasing cardiac GSH.
  • GSH supplementation significantly reduced ADR-induced cardiotoxicity markers and restored cardiac GSH levels.
  • GSH depletion exacerbated ADR cardiotoxicity, leading to severe cardiac histopathological damage.

Conclusions:

  • Glutathione (GSH) demonstrates a significant protective effect against Adriamycin (ADR)-induced cardiotoxicity.
  • GSH mitigates ADR-induced oxidative stress and preserves cardiac function and integrity.
  • GSH supplementation may represent a viable strategy to reduce the cardiotoxic side effects of ADR therapy.

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