Delayed neurological sequelae from ethylene glycol, diethylene glycol and methanol poisonings

Reddy, Nandi J.; Sudini, Madhuri; Lewis, Lionel D.

doi:10.3109/15563650.2010.532803

Cited by 52 publications

(33 citation statements)

References 36 publications

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“…Protein damage by FA is quite extensive, as evidenced by a rapid heat shock response and extensive protein polyubiquination 24 . Vulnerability of the nervous system to toxic effects of FA 18, 19, 25 is consistent with its protein-damaging properties.…”

Section: Introductionsupporting

confidence: 58%

“…These endogenous processes generate biologically significant levels of FA, as evidenced by recent mouse studies in which the loss of a maternal FA detoxification enzyme produced severe growth problems in embryos 16 and degenerative and genotoxic effects in the tissues of adult animals 17 . The metabolic production of FA is also responsible for neurotoxic effects in victims of methanol poisoning 18, 19 . FA is a common environmental toxicant with many sources of exposure, such as tobacco smoking 20 , off-gassing from consumer goods and emissions by combustion processes 15 .…”

Section: Introductionmentioning

confidence: 99%

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20S immunoproteasomes remove formaldehyde-damaged cytoplasmic proteins suppressing caspase-independent cell death

Ortega-Atienza

Krawic

Watts

et al. 2017

Sci Rep

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Immunoproteasomes are known for their involvement in antigen presentation. However, their broad tissue presence and other evidence are indicative of nonimmune functions. We examined a role for immunoproteasomes in cellular responses to the endogenous and environmental carcinogen formaldehyde (FA) that binds to cytosolic and nuclear proteins producing proteotoxic stress and genotoxic DNA-histone crosslinks. We found that immunoproteasomes were important for suppression of a caspase-independent cell death and the long-term survival of FA-treated cells. All major genotoxic responses to FA, including replication inhibition and activation of the transcription factor p53 and the apical ATM and ATR kinases, were unaffected by immunoproteasome inactivity. Immunoproteasome inhibition enhanced activation of the cytosolic protein damage sensor HSF1, elevated levels of K48-polyubiquitinated cytoplasmic proteins and increased depletion of unconjugated ubiquitin. We further found that FA induced the disassembly of 26S immunoproteasomes, but not standard 26S proteasomes, releasing the 20S catalytic immunoproteasome. FA-treated cells also had higher amounts of small activators PA28αβ and PA28γ bound to 20S particles. Our findings highlight the significance of nonnuclear damage in FA injury and reveal a major role for immunoproteasomes in elimination of FA-damaged cytoplasmic proteins through ubiquitin-independent proteolysis.

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Section: Introductionsupporting

confidence: 58%

Section: Introductionmentioning

confidence: 99%

20S immunoproteasomes remove formaldehyde-damaged cytoplasmic proteins suppressing caspase-independent cell death

Ortega-Atienza

Krawic

Watts

et al. 2017

Sci Rep

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“…In these cases, the appearance of motor deficits is slow to present and may occur weeks after initial exposure. The rigidity and bradykinesia may be partially relieved with levodopa treatment but the white matter lesions may extend beyond the basal ganglia (Reddy et al, 2010). …”

Section: Methanolmentioning

confidence: 99%

Industrial toxicants and Parkinson's disease

et al. 2012

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The exposure of the human population to environmental contaminants is recognized as a significant contributing factor for the development of Parkinson’s disease (PD) and other forms of parkinsonism. While pesticides have repeatedly been identified as risk factors for PD, these compounds represent only a subset of environmental toxicants that we are exposed to on a regular basis. Thus, non-pesticide contaminants, such as metals, solvents, and other organohalogen compounds have also been implicated in the clinical and pathological manifestations of these movement disorders and it is these non-pesticide compounds that are the subject of this review. As toxic exposures to these classes of compounds can result in a spectrum of PD or PD-related disorders, it is imperative to appreciate shared clinico-pathological characteristics or mechanisms of action of these compounds in order to further delineate the resultant disorders as well as identify improved preventive strategies or therapeutic interventions.

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“…Biotransformation of methanol may be slowing some potent inhibitors of alcohol dehydrogenase, for example by L-carnitine (Czech et al 2004). Methanol poisoning has led to Parkinsonism and polyneuropathy (Reddy et al 2010). …”

Section: Human Poisoningmentioning

confidence: 99%

Toxic Alcohols: Aliphatic Saturated Alcohols

Patočka¹,

Kuča²

2012

MMSL

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SummaryToxic alcohols that clinicians commonly encounter are ethylene glycol, methanol, and isopropanol. Adults ingest these either for suicidal intent or to achieve inebriation, since these substances are readily available and cheaper than alcohol. Nevertheless, assorted alcohols are used very often in many applications and any alcohol can be toxic if ingested in large enough quantities. Toxic alcohols discussed here include all saturated aliphatic alcohols containing from 1 to 6 carbons in their molecules.

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Delayed neurological sequelae from ethylene glycol, diethylene glycol and methanol poisonings

Cited by 52 publications

References 36 publications

20S immunoproteasomes remove formaldehyde-damaged cytoplasmic proteins suppressing caspase-independent cell death

20S immunoproteasomes remove formaldehyde-damaged cytoplasmic proteins suppressing caspase-independent cell death

Industrial toxicants and Parkinson's disease

Toxic Alcohols: Aliphatic Saturated Alcohols

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