Study on the In Vitro Effects of the Mixtures of Polycyclic Aromatic Hydrocarbons (PAHs) and Heavy Metals on Ethoxyresorufin-O-Deethylase (EROD) Activity in Mossambica tilapia Liver

Abstract

This paper reports in vitro effects of individual heavy metals (Cd(2+), Cu(2+) and Hg(2+)), and PAHs, including benzo[a]pyrene(BaP), indeno[1,2,3-cd]pyrene (IP) and fluoranthene (FL), and their mixtures on ethoxyresorufin-O-deethylase (EROD) activities using a plate-reader method. The results showed that all three metals inhibited EROD activity, while BaP/IP significantly induced the enzyme. However, FL alone decreased EROD activity. Moreover, co-treatment with BaP/IP and heavy metals inhibited PAH-induced EROD activities, while combined exposure to FL and heavy metals induced FL-inhibited EROD activities.

Genetic and epigenetic modulations in toxicity: The two-sided roles of heavy metals and polycyclic aromatic hydrocarbons from the environment

“…According to the study, the induction of CYP1A1 mRNA by heavy metal is both a transcriptional and an AhR mediated event in a manner similar to that of TCDD. To support these findings the authors established insignificant change in the CYP1A1 mRNA half-life, indicating that increase in CYP1A1 mRNA transcript in response to heavy metals were not due to a post transcriptional stabilization of the mRNA, however the metals decreased the rate of CYP1A1 protein degradation implying a posttranslational regulation of CYP1A1 by heavy metals [45] , [44] . By implication, heavy metals are capable of induing AhR expression which will result in the up-regulation of CYP1A1, and at the same time inhibit the degradation of CYP1A1 thereby increasing the half-life.…”

“…In this regards, different authors have investigated the implication of mixture of different environmental chemicals on the metabolic machinery. For instance, metalloids in combination with PAHs inhibited the induction of CYP1A1 and CYP1A2 at transcriptional and post transcriptional level [45] , [44] , [46] and consequently limited the genotoxicity of B(a)P as CYP1A1 mediated metabolism of B(a)P is prerequisite to its genotoxicity.…”