Polycyclic aromatic hydrocarbons (PAHs), dioxins, dibenzofurans, and polychlorinated biphenyls (PCBs) present in polluted environment induce cytochrome P4501A (CYP1A) isozyme in fish, which in turn results in a marked increased production of carcinogenic metabolites from PAHs. The induction of hepatic CYP1A in fish by certain classes of chemicals has been suggested as an early warning system, a "most sensitive biological response" for assessing environmental contamination conditions. This has implications for human fish consumption, as well as for the health status of aquatic organisms. Correlation between elevated CYP1A and altered steroid metabolism and decreased reproductive success has been pointed out. The induction of CYP1A and associated enzyme activities has now been confirmed in a number of field studies. Cases where these biomarkers have been studied in field conditions will be presented. Special emphasis will be given to field studies in which the induction of CYP1A activity, 7-ethoxyresorufin O-deethylase (EROD) activities and immunochemical detection of CYP1A in leaping mullet and common sole are used as a biomarker for PAH- and/or PCB-type pollutants along the Izmir Bay on the Aegean Sea.
Humans are exposed to acrylamide in their diet and cigarette smoke. Acrylamide is metabolized into glycidamide by CYP2E1. However, very few studies regarding the effects of acrylamide on cytochrome P450 and Glutathione S-Transferase (GST) isozymes have been pursued. The aim of this study is to elucidate the effects of acrylamide on cytochrome P450 and GST isozymes in HepG2 cell line. Treatment with 1.25 and 2.5 mM acrylamide caused 9.5- and 3.7-fold increases and 4.0- and 3.3-fold increases in CYP1A-associated ethoxyresorufin O-deethylase (EROD) and methoxyresorufin O-demethylase (MROD) activities, respectively. These increases were consistent with increases in mRNA and protein levels of these isozymes. Similarly, CYP2E1-associated aniline 4-hydroxylase (ANH) activity, protein levels, and mRNA levels increased 2.1- and 2.6-fold, 2.4- and 3.2-fold, and 1.4- and 1.9-fold following 1.25 and 2.5 mM acrylamide treatments, respectively. In addition, GST-mu activity was increased 2.4- and 5.1-fold by acrylamide. Moreover, GST-mu mRNA and protein levels increased twofold as a result of acrylamide treatment. In contrast, GST-pi protein and mRNA levels decreased significantly. In conclusion, human cell exposure to acrylamide causes an increase in the levels of carcinogenicity and toxicity and a disturbance in drug metabolism, possibly due to complex effects on P450 and GST isozymes.
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