Persistent organochlorinated pesticides and mechanisms of their toxicity

• Published in: Toxicology (Amsterdam) Vol. 307; pp. 74 - 88
• Main Authors: Mrema, Ezra J, Rubino, Federico M, Brambilla, Gabri, Moretto, Angelo, Tsatsakis, Aristidis M, Colosio, Claudio
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier Ireland Ltd 10-05-2013
• Subjects: adverse effects; Adverse health effect; air; air pollution; bioaccumulation; breathing; DDT (pesticide); DDT - toxicity; dibenzofuran; Emergency; Endocrine Disruptors - toxicity; endocrine system; endosulfan; Endosulfan - toxicity; Environmental Exposure - adverse effects; epigenetics; food chain; HCH (pesticide); hexachlorobenzene; Hexachlorobenzene - toxicity; Human exposure; Humans; Hydrocarbons, Chlorinated - toxicity; hydrophobicity; ingestion; Lindane - toxicity; long term effects; mechanism of action; Mechanisms of action; metabolites; Organochlorinated pesticides; oxidation; persistent organic pollutants; Pesticides - toxicity; polychlorinated biphenyls; public health; toxicity; toxicology; NO; Cytosine Guanine base pair; PCBs; Mechanisms of action; Organochlorinated pesticides; HO; superoxide radical; TCDD; polychlorinated dibenzofurans; p, p′-DDD; p, p′-DDE; GABAA; o, p′-DDD; o, p′-DDE; 1,1,1-trichloro-2-( o-chlorophenyl)-2-( p chlorophenyl)-ethane; polychlorinated biphenyls; PI3K; DDT; polychlorinated dibenzo-p-dioxins; PCDFs; 1,1-dichloro-2-( o-chlorophenyl)-2-( p-chlorophenyl)ethylene; 1,1,1-trichloro-2,2-bis(p-chlorophenyl) ethane; phosphatidylinositol 3-kinase; o, p′-DDT; O 2; beta-hexachlorocyclohexane; HCB; 1,1-dichloro-2, 2-bis (4-chlorophenyl)ethane; PCDDs; 2-OHE; Human exposure; dichlorodiphenyltrichloroethane; 2,3,7,8-tetrachlorodibenzo-p-dioxin; nitrogen oxide radical; hydroxyl radical; 1,1-dichloro-2,2-bis(p-chlorophenyl)-ethylene; 1,1-dichloro-2-( o-chlorophenyl)-2-( p chlorophenyl)ethane; gamma butyric acid type A Receptor; 6 CpG; hexachlorobenzene; 16α-OHE; 16α-hydroxyestrone; β-HCH; 2-hydroxyestrone; p, p′-DDT; Adverse health effect; O2; p,p′-DDE; o,p′-DDE; o,p′-DDD; p,p′-DDD; o,p′-DDT; p,p′-DDT
• ISSN: 0300-483X; 1879-3185
• DOI: 10.1016/j.tox.2012.11.015

Highlights ► Diet is a major source of OCP exposure for the general population. ► OCPs exposure can induce enzymes for hormones and toxicants metabolisms. ► OCPs exposure are suspected to be associated to endocrine function disruption. ► Possible toxicity mechanisms are hormone disruption, oxidative stress or epigenetic. ► Understanding of these mechanisms helps to improve public health interventions.