Thiol-reactivity of the fungicide maneb

Roede, James R.; Jones, Dean P.

doi:10.1016/j.redox.2014.04.007

Cited by 26 publications

(23 citation statements)

References 21 publications

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“…[18] Also, maneb toxicity may be mediated by ubiquitin-proteasome system inhibition,[19,20] aldehyde dehydrogenase inhibition,[21] and disruption of protein thiol functions analogous to oxidative stress. [22]…”

Section: Introductionmentioning

confidence: 99%

Of Pesticides and Men: a California Story of Genes and Environment in Parkinson’s Disease

Ritz

Paul

Bronstein³

2016

Curr Envir Health Rpt

119

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At the start of the post-genomics era, most Parkinson’s disease (PD) etiology cannot be explained by our knowledge of genetic or environmental factors alone. For more than a decade, we have explored gene-environment (GxE) interactions possibly responsible for the heterogeneity of genetic as well as environmental results across populations. We developed three pesticide exposure measures (ambient due to agricultural applications, home and garden use, occupational use) in a large population-based case-control study of incident PD in central California. Specifically, we assessed interactions with genes responsible for pesticide metabolism (PON1); transport across the blood brain barrier (ABCB1); pesticides interfering with or depending on dopamine transporter activity (DAT) and dopamine metabolism (ALDH2); impacting mitochondrial function via oxidative/nitrosative stress (NOS1) or proteasome inhibition (SKP1); and contributing to immune dysregulation (HLA-DR). These studies established some specificity for pesticides’ neurodegenerative actions, contributed biologic plausibility to epidemiologic findings, and identified genetically susceptible populations.

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Section: Introductionmentioning

confidence: 99%

Of Pesticides and Men: a California Story of Genes and Environment in Parkinson’s Disease

Ritz

Paul

Bronstein³

2016

Curr Envir Health Rpt

119

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“…Interestingly TrxR inhibition plus PQ-induced cell death or loss of TH positive neurons in animals can be reversed when cells or animals are treated with a cell permeable catalytic antioxidant indicating the role of ROS production and oxidative stress in PQ toxicity (Lopert et al 2012; Callio et al 2005; Day et al 1995; Kulich et al 2007; Patel and Day 1999). As mentioned previously, maneb can deplete thiols on Trx and combined with PQ treatment leads to potentiate the neurotoxicity of PQ (Roede and Jones 2014). Together this data indicates when mitochondrial antioxidants are depleted and DAergic cells have increased intracellular/intramitochondrial ROS production due to the redox cycling agents PQ or DQ, there is an increase in DAergic cell death as mimicking what is observed in PD.…”

Section: Antioxidants Role With Pd-redox Cycling Agentsmentioning

confidence: 87%

“…Both maneb and PQ react with complex III of the ETC and, therefore it is hypothesized that the combined treatment of both toxicants exacerbates the ROS production of PQ at complex III, causing increased mitochondrial ROS release, mitochondrial dysfunction and cell death. Additionally it has been demonstrated that maneb can deplete thiols of the antioxidant thioredoxin (Roede and Jones 2014). Depletion of either the cytosolic or mitochondrial thioredoxin system has been linked to an increase in mitochondrial dysfunction, ROS production and resulting cell death when DAergic cells are exposed to low levels of PQ (Lopert et al 2012).…”

Section: Role Of Ros Producing Toxicants and Pesticides In Pdmentioning

confidence: 99%

“…Depletion of either the cytosolic or mitochondrial thioredoxin system has been linked to an increase in mitochondrial dysfunction, ROS production and resulting cell death when DAergic cells are exposed to low levels of PQ (Lopert et al 2012). Therefore, when cells or animals are exposed to PQ and maneb, the increased ROS production at complex III with the decreased Trx/TrxR activity leads to an increase in cell death (Roede and Jones 2014; Lopert et al 2012). Other mechanisms of action have been hypothesized (alkylation, decreased glutathione levels, decreased an-tioxidant activity, neuronal excitotoxicity) and hence more research is needed to determine all the mechanisms of action that generate this synergistic and epidemiologically important effect (Roede et al 2011).…”

Section: Role Of Ros Producing Toxicants and Pesticides In Pdmentioning

confidence: 99%

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Mitochondrial mechanisms of redox cycling agents implicated in Parkinson’s disease

Lopert

Patel

2015

J Neural Transm

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Environmental agents have been implicated in Parkinson's disease (PD) based on epidemiological studies and the ability of toxicants to replicate features of PD. However, the precise mechanisms by which toxicants induce dopaminergic toxicity observed in the idiopathic form of PD remain to be fully understood. The roles of ROS and mitochondria are strongly suggested in the mechanisms by which these toxicants exert dopaminergic toxicity. There are marked differences and similarities shared by the toxicants in increasing steady-state levels of mitochondrial ROS. Furthermore, toxicants increase steady-state mitochondrial ROS levels by stimulating the production, inhibiting the antioxidant pathways of both. This review will focus on the role of mitochondria and ROS in PD associated with environmental exposures to redox-based toxicants.

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“…For example, Mn dioxide (MnO 2 ) oxidizes numerous compounds such as aromatics and alcohols [168, 169]. Compounds like maneb or mancozeb, both Mn containing fungicides, have been widely studied in toxicities and associated mechanisms [170, 171]. Lastly, methyl-cyclopentadienyl manganese tricarbonyl (MMT) is an octane enhancer added to gasoline in many countries.…”

Section: Manganese-based Compounds For Industrial and Therapeutic mentioning

confidence: 99%

Redox dynamics of manganese as a mitochondrial life-death switch

Smith

Fernandes

et al. 2017

Biochemical and Biophysical Research Communications

Self Cite

126

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Sten Orrenius, M.D., Ph.D., pioneered many areas of cellular and molecular toxicology and made seminal contributions to our knowledge of oxidative stress and glutathione (GSH) metabolism, organellar functions and Ca+2-dependent mechanisms of cell death, and mechanisms of apoptosis. On the occasion of his 80th birthday, we summarize current knowledge on redox biology of manganese (Mn) and its role in mechanisms of cell death. Mn is found in all organisms and has critical roles in cell survival and death mechanisms by regulating Mn-containing enzymes such as manganese superoxide dismutase (SOD2) or affecting expression and activity of caspases. Occupational exposures to Mn cause “manganism”, a Parkinson's disease-like condition of neurotoxicity, and experimental studies show that Mn exposure leads to accumulation of Mn in the brain, especially in mitochondria, and neuronal cell death occurs with features of an apoptotic mechanism. Interesting questions are why a ubiquitous metal that is essential for mitochondrial function would accumulate to excessive levels, cause increased H2O2 production and lead to cell death. Is this due to the interactions of Mn with other essential metals, such as iron, or with toxic metals, such as cadmium? Why is the Mn loading in the human brain so variable, and why is there such a narrow window between dietary adequacy and toxicity? Are non-neuronal tissues similarly vulnerable to insufficiency and excess, yet not characterized? We conclude that Mn is an important component of the redox interface between an organism and its environment and warrants detailed studies to understand the role of Mn as a mitochondrial life-death switch.

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Thiol-reactivity of the fungicide maneb

Cited by 26 publications

References 21 publications

Of Pesticides and Men: a California Story of Genes and Environment in Parkinson’s Disease

Of Pesticides and Men: a California Story of Genes and Environment in Parkinson’s Disease

Mitochondrial mechanisms of redox cycling agents implicated in Parkinson’s disease

Redox dynamics of manganese as a mitochondrial life-death switch

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