Pharmacotoxicology entails the study of the consequences of toxic exposure to pharmaceutical drugs and agents in the health care field.
A very common mechanism is covalent binding of either the drug or its metabolites to specific enzymes or receptor in tissue-specific pathways that then will elicit toxic responses.
To avoid toxicity during treatment, many times the drug needs to be changed to target a different aspect of the illness or symptoms.
Tamoxifen, a selective estrogen receptor modulator, has been shown to alter the humoral adaptive immune response in gilthead seabream.
If a drug can bind to unexpected proteins, receptors, or enzymes that can alter different pathways other than those desired for treatment, severe downstream effects can develop.
Acetaminophen is metabolized by CYP2E1 to produce NAPQI, which then causes significant oxidative stress due to increased reactive oxygen species (ROS).
This could either cause reactive intermediates/drug activity to persist for longer than necessary, or the drug will be cleared quicker than normal and prevent any therapeutic actions from occurring.
Overdoses or treatments in conjunction with other NSAIDs can produce additive effects, which can lead to increased oxidative stress and ROS activity.
Chronic exposure or overdose of these pharmaceuticals can lead to serotonin and CNS hyperexcitation, weight changes, and, in severe cases, suicide.
[7] Other anti-cancer drugs, such as fluoropyrimidines and taxanes, are extremely effective at treating and reducing tumor proliferation, but have high incidences of cardiac arrhythmias and myocardial infarctions.