Cardiotoxicity in rats induced by methidathion and ameliorating effect of vitamins E and C

Turhan Yavuz1, Irfan Altuntas, Namik Delibas

  • 1Department of Cardiovascular Surgery, School of Medicine, Suleyman Demirel University, Isparta, Turkey. turhan.kvc@doctor.com

Insights

Subchronic methidathion exposure causes heart damage, indicated by increased malondialdehyde and cardiac troponin I. Co-administration of vitamins E and C significantly reduced this methidathion-induced cardiotoxicity.

Area of Science:

  • Toxicology
  • Cardiology
  • Biochemistry

Background:

  • Organophosphate pesticides like methidathion (MD) can cause toxicity.
  • Oxidative stress and cardiac damage are potential consequences of pesticide exposure.

Purpose of the Study:

  • To investigate the cardiotoxic effects of subchronic methidathion (MD) administration.
  • To evaluate the protective potential of combined vitamin E and vitamin C against MD-induced heart damage.

Main Methods:

  • Rats were divided into control, MD-treated, and MD + vitamins E and C groups.
  • MD was administered daily for four weeks; vitamins were given post-MD treatment.
  • Assessed heart tissue malondialdehyde (MDA), serum cardiac troponin I (TnI), and cholinesterase (ChE) activity.
  • Histopathological examination of heart tissue was performed.

Main Results:

  • MD significantly increased MDA and TnI levels and decreased ChE activity.
  • MD caused significant histopathological changes in heart tissue.
  • Combined vitamins E and C significantly attenuated MD-induced increases in MDA and TnI, and mitigated histopathological damage.
  • Vitamins E and C also lessened the decrease in ChE activity caused by MD.

Conclusions:

  • Subchronic methidathion administration induces significant cardiotoxicity.
  • Concurrent administration of vitamins E and C effectively reduces methidathion-induced heart damage and oxidative stress.

Related Concept Videos

Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...