Related Experiment Video
Updated: Oct 16, 2026

Experimental Protocol for Detecting Mitochondrial Function in Hepatocytes Exposed to Organochlorine Pesticides
Published on: September 16, 2020
Mitochondrial targets of drug toxicity
1Department of Biochemistry and Molecular Biology, University of Minnesota School of Medicine, Duluth 55812, USA. kwallace@d.umn.edu
Abstract:
Mitochondria have long been recognized as the generators of energy for the cell. Like any other power source, however, mitochondria are highly vulnerable to inhibition or uncoupling of the energy harnessing process and run a high risk for catastrophic damage to the cell. The exquisite structural and functional characteristics of mitochondria provide a number of primary targets for xenobiotic-induced bioenergetic failure. They also provide opportunities for selective delivery of drugs to the mitochondrion. In light of the large number of natural, commercial, pharmaceutical, and environmental chemicals that manifest their toxicity by interfering with mitochondrial bioenergetics, it is important to understand the underlying mechanisms. The significance is further underscored by the recent identification of bioenergetic control points for cell replication and differentiation and the realization that mitochondria play a determinant role in cell signaling and apoptotic modes of cell death.
Related Concept Videos
Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...
Targets for Drug Action: Overview
Receptors are either membrane-spanning or intracellular proteins, which upon binding a ligand, get activated and transmit the signal downstream to elicit a response. Drugs bind receptors, either mimicking the action of endogenous ligands or blocking the receptor activity to bring about a modified response. Nearly 35% of approved drugs target the G...
Drug Toxicity: Dose-Dependent Reactions
The Electron Transport Chain
Inhibitors of the electron transport chain
Rotenone, a widely used pesticide, prevents electron transfer from Fe-S cluster to ubiquinone or Q in...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
Drug toxicity: Drug–Drug Interaction
