Phytotherapeutic approach: a new hope for polycyclic aromatic hydrocarbons induced cellular disorders, autophagic and apoptotic cell death

Abstract

Polycyclic aromatic hydrocarbons (PAHs) comprise the major class of cancer-causing chemicals and are ranked ninth among the chemical compounds threatening to humans. Moreover, interest in PAHs has been mainly due to their genotoxic, teratogenic, mutagenic and carcinogenic property. Polymorphism in cytochrome P450 (CYP450) and aryl hydrocarbon receptor (AhR) has the capacity to convert procarcinogens into carcinogens, which is an imperative factor contributing to individual susceptibility to cancer development. The carcinogenicity potential of PAHs is related to their ability to bind to DNA, thereby enhances DNA cross-linking, causing a series of disruptive effects which can result in tumor initiation. They induce cellular toxicity by regulating the generation of reactive oxygen species (ROS), which arbitrate apoptosis. Additionally, cellular toxicity-mediated apoptotic and autophagic cell death and immune suppression by industrial pollutants PAH, provide fertile ground for the proliferation of mutated cells, which results in cancer growth and progression. PAHs play a foremost role in angiogenesis necessary for tumor metastasization by promoting the upregulation of metalloproteinase-9 (MMP-9), vascular endothelial growth factor (VEGF) and hypoxia inducible factor (HIF) in human cancer cells. This review sheds light on the molecular mechanisms of PAHs induced cancer development as well as autophagic and apoptotic cell death. Besides that authors have unraveled how phytotherapeutics is an alternate potential therapeutics acting as a savior from the toxic effects of PAHs for safer and cost effective perspectives.

Casp8 hypomethylation and neural tube defects in association with polycyclic aromatic hydrocarbon exposure

“…Increased levels of caspase-8 and ROS have both been detected in hyperglycemia-induced NTDs, and antioxidants could ameliorate NTD occurrence with decreased caspase-8 cleavage [14, 16]. In addition, ROS generation induced by PAHs has been identified as a mechanism of PAH-mediated apoptosis [27]. However, the full spectrum of the links from PAH exposure, oxidative stress, CASP8/Casp8 methylation change, caspase-8 activation, apoptosis, to NTD formation has not yet been fully explored.…”

Serum VEGF Level Is Different in Adolescents Smoking Waterpipe versus Cigarettes: The Irbid TRY

“…In addition, the toxicant profiles of Cg and Wp have been shown to be different. For example, Wp smoke contains high levels of polyaromatic hydrocarbons (PAHs), volatile aldehyde, and CO than that of Cg smoke [34], which might modulate VEGF expression [35,36,37,38,39]. Furthermore, compared to Cg, additional toxicants are derived from charcoal, flavors, added sugars, and glycerol that are in Wp smoke [40].…”

Organochlorine pesticides, brominated flame retardants, synthetic musks and polycyclic aromatic hydrocarbons in shrimps. An overview of occurrence and its implication on human exposure

“…In terms of human exposure, PAHs have been reported to be carcinogenic, mutagenic and teratogenic [24]. The most significant endpoint of PAH toxicity after long term exposure is cancer, they can lead to proliferation of mutated cells resulting in cancer growth [26]. Furthermore, they have been reported to have endocrine disruptor capacity [27].…”