TitleBehavioral and Cognitive Performance Following Exposure to Second-Hand Smoke (SHS) from Tobacco Products Associated with Oxidative-Stress-Induced DNA Damage and Repair and Disruption of the Gut Microbiome.
Publication TypeJournal Article
Year of Publication2023
AuthorsRaber, J, Stagaman, K, Kasschau, KD, Davenport, C, Lopes, L, Nguyen, D, Torres, ERuth, Sharpton, TJ, Kisby, G
JournalGenes (Basel)
Date Published2023 Aug 27
KeywordsAnimals, Cognition, DNA Damage, Gastrointestinal Microbiome, Humans, Infant, Mice, Oxidative Stress, Tobacco, Tobacco Products, Tobacco Smoke Pollution

Exposure to second-hand Smoke (SHS) remains prevalent. The underlying mechanisms of how SHS affects the brain require elucidation. We tested the hypothesis that SHS inhalation drives changes in the gut microbiome, impacting behavioral and cognitive performance as well as neuropathology in two-month-old wild-type (WT) mice and mice expressing wild-type human tau, a genetic model pertinent to Alzheimer's disease mice, following chronic SHS exposure (10 months to ~30 mg/m). SHS exposure impacted the composition of the gut microbiome as well as the biodiversity and evenness of the gut microbiome in a sex-dependent fashion. This variation in the composition and biodiversity of the gut microbiome is also associated with several measures of cognitive performance. These results support the hypothesis that the gut microbiome contributes to the effect of SHS exposure on cognition. The percentage of 8-OHdG-labeled cells in the CA1 region of the hippocampus was also associated with performance in the novel object recognition test, consistent with urine and serum levels of 8-OHdG serving as a biomarker of cognitive performance in humans. We also assessed the effects of SHS on the percentage of p21-labeled cells, an early cellular marker of senescence that is upregulated in bronchial cells after exposure to cigarette smoke. Nuclear staining of p21-labeled cells was more prominent in larger cells of the prefrontal cortex and CA1 hippocampal neurons of SHS-exposed mice than in sham-exposed mice, and there was a significantly greater percentage of labelled cells in the prefrontal cortex and CA1 region of the hippocampus of SHS than air-exposed mice, suggesting that exposure to SHS may result in accelerated brain aging through oxidative-stress-induced injury.

Alternate JournalGenes (Basel)
PubMed ID37761842
PubMed Central IDPMC10531154
Grant ListR21 ES027943 / ES / NIEHS NIH HHS / United States
R01 AG030226 / AG / NIA NIH HHS / United States
P30 ES030287 / ES / NIEHS NIH HHS / United States
T32 AG055378 / AG / NIA NIH HHS / United States
R01 ES030226 / ES / NIEHS NIH HHS / United States