TY - JOUR
TI - CYP polymorphisms and pathological conditions related to chronic exposure to organochlorine pesticides
AU - Docea, A.O.
AU - Vassilopoulou, L.
AU - Fragou, D.
AU - Arsene, A.L.
AU - Fenga, C.
AU - Kovatsi, L.
AU - Petrakis, D.
AU - Rakitskii, V.N.
AU - Nosyrev, A.E.
AU - Izotov, B.N.
AU - Golokhvast, K.S.
AU - Zakharenko, A.M.
AU - Vakis, A.
AU - Tsitsimpikou, C.
AU - Drakoulis, N.
JO - Toxicology Reports
PY - 2017
VL - 4
TODO - null
SP - 335-341
PB - ELSEVIER SCIENCE INC 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN - 2214-7500
TODO - 10.1016/j.toxrep.2017.05.007
TODO - cytochrome P450;  cytochrome P450 1A1;  cytochrome P450 2C11;  cytochrome P450 2C19;  cytochrome P450 2C9;  cytochrome P450 2D6;  cytochrome P450 3A4;  methoxychlor;  organochlorine pesticide;  phenoxyacetic acid;  reactive oxygen metabolite, breast cancer;  cancer risk;  carcinogenesis;  carcinogenicity;  cholesterol synthesis;  cytochrome P450 gene;  DNA polymorphism;  DNA repair;  drug metabolism;  drug transformation;  environmental factor;  enzyme activity;  estrogen metabolism;  gene;  gene mutation;  gene overexpression;  genetic variation;  human;  liver failure;  long term exposure;  nonhuman;  Parkinson disease;  priority journal;  prostate hypertrophy;  restriction fragment length polymorphism;  Review;  signal transduction;  single nucleotide polymorphism;  sperm quality;  spermatozoon motility;  xenobiotic metabolism
TODO - The association between genetic variations in the cytochrome P450 (CYP) family genes and pathological conditions related to long-term exposure to organochlorine compounds (OCs) deserves further elucidation. OCs are persistent organic pollutants with bioaccumulative and lipophilic characteristics. They can act as endocrine disruptors and perturb cellular mechanisms. Prolonged exposure to OCs has been associated with different pathological manifestations. CYP genes are responsible for transcribing enzymes essential in xenobiotic metabolism. Therefore, polymorphisms in these genetic sequences a. alter the metabolic pathways, b. induce false cellular responses, and c. may provoke pathological conditions. The main aim of this review is to define the interaction between parameters a, b and c at a mechanistic/molecular level, with references in clinical cases. © 2017 The Authors
ER -