Effects of Environmental Tobacco Smoke on Adult Rat Brain Biochemistry

Abstract

Environmental tobacco smoke (ETS) has been linked to deleterious health effects, particularly pulmonary and cardiac disease; yet, the general public considers ETS benign to brain function in adults. In contrast, epidemiological data have suggested that ETS impacts the brain and potentially modulates neurodegenerative disease. The present study begins to examine yet unknown biochemical effects of ETS on the adult mammalian brain. In the developed animal model, adult male rats were exposed to ETS 3 h a day for 3 weeks. Biochemical data showed altered glial fibrillary acid protein levels as a main treatment effect of ETS, suggestive of reactive astrogliosis. Yet, markers of oxidative and cell stress were unaffected by ETS exposure in the brain regions examined. Increased proteolytic degradation of αII-spectrin by caspase-3 and the dephosphorylation of serine 116 on PEA-15 indicated greater apoptotic cell death modulated by the extrinsic pathway in the brains of ETS-exposed animals. Further, β-synuclein was upregulated by ETS, a neuroprotective protein previously reported to exhibit anti-apoptotic and anti-fibrillogenic properties. These findings demonstrate that ETS exposure alters the neuroproteome of the adult rat brain, and suggest modulation of inflammatory and cell death processes.

Cigarette Smoking Accelerated Brain Aging and Induced Pre-Alzheimer-Like Neuropathology in Rats

“…This data is consistent with a report showing elevation of oxidative stress in the hippocampus of 60-day cigarette smoke-exposed mice [17]. Although another study conducted by Fuller and colleagues showed no change in oxidative stress levels in the brain of cigarette smoke-exposed rats [34], we believe the experimental protocol which determined the amount of cigarette smoke being taken was responsible for the observed discrepant findings. In their study, rats were exposed to cigarette smoke 3 h daily for 3 weeks to mimic airborne exposure as experienced in a household room, with a smoker consuming two cigarettes per hour over 10 h. While apoptotic cell death and increased activities of capsase-3 were found in their model, our model did not induce activation of caspase-3 nor neuronal cell loss as revealed by Nissl staining (data not shown).…”

Exposure of Rats to Environmental Tobacco Smoke during Cerebellar Development Alters Behavior and Perturbs Mitochondrial Energetics

“…The functional deficits seen in ETS-exposed children suggest perturbation to circuits involving multiple brain regions, and indeed we previously observed change in the frontal cortex, hippocampus, and cerebellum after modeled adult ETS exposure (Fuller et al 2010). However, the mechanistic studies here warranted anatomical focus.…”

“…Pregnant Sprague-Dawley rats were purchased from Harlan Laboratories (Indianapolis, IN) and housed in a facility approved by the Association for Assessment and Accreditation of Laboratory Animal Care on a 12-hr light cycle with ad libitum access to food and water. We treated male rat pups daily from age PD8 to PD23 in a Teague TE-10 smoking system (Teague Enterprises, Woodland, CA) operated as described previously (Fuller et al 2010; Gospe et al 1996; Slotkin et al 2001), with TSP levels confirmed daily. The first of two exposure groups received amplified ETS at a mean daily level of 300 µg/m 3 TSP (ETS 300 ), with peak concentrations of 2 mg/m 3 during active smoking.…”

Cigarette Smoke-Induced Cerebral Cortical Interleukin-6 Elevation is not Mediated Through Oxidative Stress

“…In our model, we observed no significant changes in the expression of Iba-1 or GFAP in cortex after CS exposure, which is consistent with the earlier literature (Fig. 2, Fuller et al 2010). These findings suggest that the inflammatory pathway had not yet been activated even when IL-6 levels were elevated in our model.

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