Academic Editor: Vesna Jacevic
Aluminum, arsenic, cadmium, chromium, cobalt, copper, iron, lead, mercury,
nickel, thallium, titanium, zinc, carbon tetrachloride, phthalates, glyphosate,
alcohol, drugs, and herbs are under discussion having the potential to injure the
human liver, but allocation of the injury to the hepatotoxicant as exact cause is
difficult for physicians and requires basic clinical knowledge of toxicology
details. Liver injury occurs at a variable extent depending on the dose, mostly
reproducible in animal models that allow studies on molecular steps leading to
the hepatocellular injury. These exogenous hepatotoxins may cause an
overproduction of reactive oxidative species (ROS), which are generated during
microsomal or mitochondrial oxidative stress from incomplete oxygen split and
trigger the injury if protective antioxidant capacities are reduced. Primary
subcelluar target organelles involved are liver mitochondria through lipid
peroxidation of membrane structures and the action of free radicals such as
singlet radical