Acetaminophen chemical structure

Bioactivation is a classic toxicity mechanism where the functional group or the chemical structure of the drug molecule is altered by enzymatic reactions. For example, the enzymatic breakdown of the analgesic acetaminophen (paracetamol), where the aromatic nature and the hydroxyl functionality in paracetamol are lost, yields A -acetyl-p-benzoquinone imine, a hepatotoxic agent. Paracetamol can cause liver damage and even liver failure, especially when combined with alcohol. 

Oxycodone is available alone or in combination with either acetaminophen or aspirin. Its chemical structure is most closely related to codeine, but it has strong painkilling effects equal to those of morphine. 

Fig. 37.7 (a) Chemical structures of acetaminophen and p-amidophenol-modified calix[4]arene (b) Snapshot of the interfacial crystallization of acetaminophen at the air-water interface (Reproduced with permission from Ref [34], Copyright 2011, American Chemical Society)... 

Isomalt has very good thermal and chemical stability. When it is melted, no changes in the molecular structure are observed. It exhibits considerable resistance to acids and microbial influences. Isomalt is non-hygroscopic, and at 25°C does not significantly absorb additional water up to a relative humidity (RH) of 85 paracetamol (acetaminophen) tablets based on isomalt were stored for 6 months at 85% RH at 20°C and retained their physical aspect. ... 

Currently, over 100 compounds have been identified as PPs. The literature indicates that induction of peroxisome proliferation is not limited to exogenous chemicals. A number of endogenous substances, such as the steroid hormones, thyroid hormones, mor-phogenes, and fatty acids, are also involved in peroxisome proliferation. Peroxisome proliferation in hepatic parenchymal cells of rats and mice following the administration of clofibrate has been reported by numerous investigators. Compounds that are structurally unrelated to clofibrate, such as acetaminophen and Wy-14,643, can also cause peroxisome proliferation (Table 1). The industrial solvent trichloroethylene, the industrial plasticizers dill-ethyl hexyl) phthalate (DEHP) and di(2-ethyl hexyl) adipate (DEHA), have also been found to be hepatic peroxisome proliferators. 

Although drugs such as acetaminophen bind to AhR, the majority of AhR agonists or antagonists are environmental chemicals. Polychlorinated diben-zodioxins such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), dibenzofu-rans, biphenyls, and a number of other chemicals are widespread pollutants in aquatic ecosystems. These compounds cause a high reproductive and developmental toxicity, which is mediated via binding to the AhR. Thus they pose a serious threat to many populations of mammals, birds, and fish. Various adverse effects—including structural malformations, reduced fertility, tumor promotion, immunotoxicity, and skin disorders like chloracne—have been observed [139]. 

---