PMID- 25271248 OWN - NLM STAT- MEDLINE DCOM- 20160307 LR - 20150211 IS - 1470-2738 (Electronic) IS - 0143-005X (Linking) VI - 69 IP - 3 DP - 2015 Mar TI - Hormesis and public health: can glutathione depletion and mitochondrial dysfunction due to very low-dose chronic exposure to persistent organic pollutants be mitigated? PG - 294-300 LID - 10.1136/jech-2014-203861 [doi] AB - Exposure to persistent organic pollutants (POPs) is linked to many chronic diseases, including diabetes and cardiovascular diseases. Among several possible mechanisms are gradual glutathione depletion and mitochondrial dysfunction after chronic exposure to very low doses of POP mixtures. However, it is biologically noteworthy that glutathione status and mitochondrial function is subject to hormesis, defined broadly as mild stress-induced stimulation of cellular protective mechanisms, including increased synthesis of glutathione and promotion of mitochondrial biogenesis. Although high levels of reactive oxygen/nitrogen species (ROS) can cause cellular damage, certain levels of ROS function as signalling molecules to induce hormetic effects. Thus, similar to many other stressors generating ROS, glutathione status and mitochondrial function can be improved at higher POP doses. However, higher POP levels are dangerous despite their hormetic effects due to other adverse phenomena. Also, the persistent nature of POPs can make hormetic effects less effective in humans as hormesis may be the most active with transient stressors. Hormesis-inducing stressors should be placed into three categories for public health purposes: (1) disadvantageous: chemicals like POPs and radiation, that could harm humans by endocrine disruption, action of chemical mixtures and susceptible populations; (2) neutral: cold, heat, and gravity; and (3) advantageous: moderate exercise, phytochemical intake, and calorie restriction. Noting that regulation of POPs, while critical, has provided insufficient protection because POPs persist in human bodies and the food chain, advantageous stressors should be used by the public to mitigate glutathione depletion and mitochondrial dysfunction due to POPs. CI - Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions. FAU - Lee, Duk-Hee AU - Lee DH AD - Department of Preventive Medicine, School of Medicine, Kyungpook National University, Daegu, Korea Department of Biomedical Science, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University, Daegu, Korea. FAU - Jacobs, David R Jr AU - Jacobs DR Jr AD - Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, Minnesota, USA. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Review DEP - 20140930 PL - England TA - J Epidemiol Community Health JT - Journal of epidemiology and community health JID - 7909766 RN - 0 (Environmental Pollutants) RN - 0 (Organic Chemicals) RN - GAN16C9B8O (Glutathione) SB - IM MH - Age Factors MH - Animals MH - Chronic Disease MH - Environmental Exposure/*adverse effects/prevention & control MH - Environmental Pollutants/*adverse effects MH - Glutathione/*deficiency MH - Hormesis/*drug effects/physiology MH - Humans MH - Mitochondria/*drug effects/physiology MH - Organic Chemicals/adverse effects MH - Oxidative Stress/*drug effects/physiology MH - *Public Health OTO - NOTNLM OT - CHRONIC DI OT - ENVIRONMENTAL HEALTH OT - HEALTH PROMOTION OT - PUBLIC HEALTH EDAT- 2014/10/02 06:00 MHDA- 2016/03/08 06:00 CRDT- 2014/10/02 06:00 PHST- 2014/10/02 06:00 [entrez] PHST- 2014/10/02 06:00 [pubmed] PHST- 2016/03/08 06:00 [medline] AID - jech-2014-203861 [pii] AID - 10.1136/jech-2014-203861 [doi] PST - ppublish SO - J Epidemiol Community Health. 2015 Mar;69(3):294-300. doi: 10.1136/jech-2014-203861. Epub 2014 Sep 30.