ArticleInhalation toxicology2010
Differential inhibition of mitochondrial respiratory complexes by inhalation of combustion smoke and carbon monoxide, in vivo, in the rat brain.
Article in Inhalation toxicology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Dose-dependent cerebral metabolic impairment in a swine model of carbon monoxide poisoning.Neurotoxicology · 2026Article
- Robust differential gene expression patterns in the prefrontal cortex of male mice exposed to an occupationally relevant dose of laboratory-generated wildfire smoke.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Elevated Neuroglobin Lessens Neuroinflammation and Alleviates Neurobehavioral Deficits Induced by Acute Inhalation of Combustion Smoke in the Mouse.Neurochemical research · 2019Article
- Nicotine mediates expression of genes related to antioxidant capacity and oxidative stress response in HIV-1 transgenic rat brain.Journal of neurovirology · 2016Article
- Cigarette toxicity triggers Leber's hereditary optic neuropathy by affecting mtDNA copy number, oxidative phosphorylation and ROS detoxification pathways.Cell death & disease · 2015Article
- Neuroglobin mitigates mitochondrial impairments induced by acute inhalation of combustion smoke in the mouse brain.Inhalation toxicology · 2014Article
- Transgenic overexpression of neuroglobin attenuates formation of smoke-inhalation-induced oxidative DNA damage, in vivo, in the mouse brain.Free radical biology & medicine · 2011Article
- Acute inhalation of combustion smoke triggers neuroinflammation and persistent anxiety-like behavior in the mouse.Inhalation toxicologyArticle
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Combustion smoke contains gases and particulates, which act via hypoxia and cytotoxicity producing mechanisms to injure cells and tissues. While carbon monoxide (CO) is the major toxicant in smoke, its toxicity is exacerbated in the presence of other compounds. Here, we examined modulations of mitochondrial and cytosolic energy metabolism by inhalation of combustion smoke versus CO, in vivo, in the rat brain. Measurements revealed reduced activities of respiratory chain (RC) complexes, with greater inhibition by smoke than equivalent CO in ambient air. In the case of RC complex IV, inhibition by CO and smoke was similar--suggesting that complex IV inhibition is primarily by the action of CO. In contrast, inhibition of complexes I and III was greater by smoke. Increases in cytosolic lactate dehydrogenase and pyruvate kinase activities accompanied inhibition of RC complexes, likely reflecting compensatory increases in cytosolic energy production. Together, the data provide new insights into the mechanisms of smoke inhalation-induced perturbations of brain energetics, which impact neuronal function and contribute to the development of neuropathologies in survivors of exposures to CO and combustion smoke.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.