The body removes xenobiotics by
xenobiotic metabolism. This consists of the deactivation and the excretion of xenobiotics and happens mostly in the liver. Excretion routes are urine, feces, breath, and sweat. Hepatic enzymes are responsible for the metabolism of xenobiotics by first activating them (oxidation, reduction, hydrolysis, and/or hydration of the xenobiotic), and then conjugating the active secondary metabolite with
glucuronic acid,
sulfuric acid, or
glutathione, followed by excretion in bile or urine. An example of a group of enzymes involved in xenobiotic metabolism is hepatic microsomal
cytochrome P450. These enzymes that metabolize xenobiotics are very important for the pharmaceutical industry because they are responsible for the breakdown of medications. A species with this unique cytochrome P450 system is
Drosophila mettleri, which uses xenobiotic resistance to exploit a wider nesting range including both soil moistened with necrotic exudates and necrotic plots themselves. Although the body is able to remove xenobiotics by reducing it to a less toxic form through xenobiotic metabolism then excreting it, it is also possible for it to be converted into a more toxic form in some cases. This process is referred to as
bioactivation and can result in structural and functional changes to the microbiota. Exposure to xenobiotics can disrupt the microbiome community structure, either by increasing or decreasing the size of certain bacterial populations depending on the substance. Functional changes that result vary depending on the substance and can include increased expression in genes involved in stress response and
antibiotic resistance, changes in the levels of metabolites produced, etc. Organisms can also
evolve to tolerate xenobiotics. An example is the
co-evolution of the production of
tetrodotoxin in the
rough-skinned newt and the evolution of tetrodotoxin resistance in its predator, the
Common Garter Snake. In this predator–prey pair, an
evolutionary arms race has produced high levels of toxin in the newt and correspondingly high levels of resistance in the snake. This evolutionary response is based on the snake evolving modified forms of the
ion channels that the toxin acts upon, so becoming resistant to its effects. Another example of a xenobiotic tolerance mechanism is the use of
ATP-binding cassette (ABC) transporters, which is largely exhibited in insects. Such transporters contribute to resistance by enabling the transport of toxins across the cell membrane, thus preventing accumulation of these substances within cells. ==Xenobiotics in the environment==