Holding the specialized journal club entitled "Drug-induced mitochondrial dysfunction and cardiotoxicity"

  • 12/26/18 12:16 PM
  • Sepideh Dashti

Instructor: Dr Ahmad Salimi (Asistant professor of Toxicology)

Date: Wednesday, January 9, 2019

Start Time: 10:00

Venue: Meeting Room

* For faculties

Presentation language: English

Abstract

Mitochondria has an essential role in myocardial tissue homeostasis; thus, deterioration in mitochondrial function eventually leads to cardiomyocyte and endothelial cell death and consequent cardiovascular dysfunction. Several chemical compounds and drugs shave been known to directly or indirectly modulate cardiac mitochondrial function, which can account both for the toxicological and pharmacological properties of these substances. In many cases, toxicity problems appear only in the presence of additional cardiovascular disease conditions are developed months/years following the exposure, making the diagnosis difficult. Cardiotoxic agents affecting mitochondria include several widely used anticancer drugs such as doxorubicin, cisplatin, trastuzumab, arsenic trioxide, mitoxantrone, imatinib, bevacizumab, sunitinib, and sorafenib, antiviral compound azidothymidine and several oral antidiabetics. Illicit drugs such as alcohol, cocaine, methamphetamine, ecstasy, and synthetic cannabinoids (spice, K2) may also induce mitochondria-related cardiotoxicity. Mitochondrial toxicity develops due to various mechanisms involving interference with the mitochondrial respiratory chain or inhibition of the important mitochondrial enzymes. The final phase of mitochondrial dysfunction induces loss of mitochondrial membrane potential and an increase in mitochondrial oxidative/nitrative stress, eventually culminating into cell death.