Mitochondrial Redox Dysfunction and Environmental Exposures

Caito, Samuel; Aschner, Michael

doi:10.1089/ars.2015.6289

Cited by 71 publications

(65 citation statements)

References 205 publications

(183 reference statements)

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“…Among environmental pollutants, Pb is a paradigmatic example of a developmental neurotoxicant able to interfere with developmental programming through different and possibly interrelated mechanisms. These include the antagonism of NMDA receptors in the early developmental phases, which is the key event at the basis of Pb interference with synaptogenesis, neural network formation, and behavioral plasticity (Toscano and Guilarte 2005), but Pb also induces latent changes in antioxidant defenses and mitochondrial redox dysfunction that may trigger neurodegeneration-related pathways at later life stages (Caito and Aschner 2015).…”

Section: Resultsmentioning

confidence: 99%

Early-Life Toxic Insults and Onset of Sporadic Neurodegenerative Diseases—an Overview of Experimental Studies

Tartaglione

Venerosi

Calamandrei

2015

Current Topics in Behavioral Neurosciences

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The developmental origin of health and disease hypothesis states that adverse fetal and early childhood exposures can predispose to obesity, cardiovascular, and neurodegenerative diseases (NDDs) in adult life. Early exposure to environmental chemicals interferes with developmental programming and induces subclinical alterations that may hesitate in pathophysiology and behavioral deficits at a later life stage. The mechanisms by which perinatal insults lead to altered programming and to disease later in life are still undefined. The long latency between exposure and onset of disease, the difficulty of reconstructing early exposures, and the wealth of factors which the individual is exposed to during the life course make extremely difficult to prove the developmental origin of NDDs in clinical and epidemiological studies. An overview of animal studies assessing the long-term effects of perinatal exposure to different chemicals (heavy metals and pesticides) supports the link between exposure and hallmarks of neurodegeneration at the adult stage. Furthermore, models of maternal immune activation show that brain inflammation in early life may enhance adult vulnerability to environmental toxins, thus supporting the multiple hit hypothesis for NDDs' etiology. The study of prospective animal cohorts may help to unraveling the complex pathophysiology of sporadic NDDs. In vivo models could be a powerful tool to clarify the mechanisms through which different kinds of insults predispose to cell loss in the adult age, to establish a cause-effect relationship between "omic" signatures and disease/dysfunction later in life, and to identify peripheral biomarkers of exposure, effects, and susceptibility, for translation to prospective epidemiological studies.

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Section: Resultsmentioning

confidence: 99%

Early-Life Toxic Insults and Onset of Sporadic Neurodegenerative Diseases—an Overview of Experimental Studies

Tartaglione

Venerosi

Calamandrei

2015

Current Topics in Behavioral Neurosciences

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“…Respiratory dysregulation has been linked to cell death and helps increase the onset of neurodegenerative diseases, such as PD and AD. The mechanisms underlying the sensitivity of the mitochondrial respiratory complexes to redox modulation, as well as the effects of environmental contaminants that have mitochondrial toxicity, have recently been examined and discussed [87]. Protection of mitochondria against damage due to specific xenobiotics can be a useful tool to help avoid disease.…”

Section: Concomitant Treatment With Antioxidantsmentioning

confidence: 99%

Rationale for the Successful Management of EDTA Chelation Therapy in Human Burden by Toxic Metals

Ferrero

2016

BioMed Research International

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Exposure to environmental and occupational toxicants is responsible for adverse effects on human health. Chelation therapy is the only procedure able to remove toxic metals from human organs and tissue, aiming to treat damage related to acute and/or chronic intoxication. The present review focuses on the most recent evidence of the successful use of the chelating agent ethylenediaminetetraacetic acid (EDTA). Assessment of toxic-metal presence in humans, as well as the rationale of EDTA therapy in cardiovascular and neurodegenerative diseases, is reported.

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“…Decreased ATP production and oxidative stress are important factors in methyl mercury toxicity (Ally et al, ; Caito and Aschner, ). The general role of mercury and oxidative stress is nicely summarized in Tinkov et al ().…”

Section: Mitochondria and Oxidative Stressmentioning

confidence: 99%

Effects of methyl mercury exposure on pancreatic beta cell development and function

Schumacher

Abbott

2016

J of Applied Toxicology

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Methyl mercury is an environmental contaminant of worldwide concern. Since the discovery of methyl mercury exposure due to eating contaminated fish as the underlying cause of the Minamata disaster, the scientific community has known about the sensitivity of the developing central nervous system to mercury toxicity. Warnings are given to pregnant women and young children to limit consumption of foods containing methyl mercury to protect the embryonic, fetal and postnatally developing central nervous system. However, evidence also suggests that exposure to methyl mercury or various forms of inorganic mercury may also affect development and function of other organs. Numerous reports indicate a worldwide increase in diabetes, particularly type 2 diabetes. Quite recently, methyl mercury has been shown to have adverse effects on pancreatic beta (β) cell development and function, resulting in insulin resistance and hyperglycemia and may even lead to the development of diabetes. This review discusses possible mechanisms by which methyl mercury exposure may adversely affect pancreatic β cell development and function, and the role that methyl mercury exposure may have in the reported worldwide increase in diabetes, particularly type 2 diabetes. While additional information is needed regarding associations between mercury exposure and specific mechanisms of the pathogenesis of diabetes in the human population, methyl mercury's adverse effects on the body's natural sources of antioxidants suggest that one possible therapeutic strategy could involve supplementation with antioxidants. Thus, it is important that additional investigation be undertaken into the role of methyl mercury exposure and reduced pancreatic β cell function. Copyright © 2016 John Wiley & Sons, Ltd.

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Mitochondrial Redox Dysfunction and Environmental Exposures

Cited by 71 publications

References 205 publications

Early-Life Toxic Insults and Onset of Sporadic Neurodegenerative Diseases—an Overview of Experimental Studies

Early-Life Toxic Insults and Onset of Sporadic Neurodegenerative Diseases—an Overview of Experimental Studies

Rationale for the Successful Management of EDTA Chelation Therapy in Human Burden by Toxic Metals

Effects of methyl mercury exposure on pancreatic beta cell development and function

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