Effects of 28-day nose-only inhalation of PCB52 (2,2′,5,5′-Tetrachlorobiphenyl) on the brain transcriptome
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PROVIDER: PRJNA1033623 | ENA |
REPOSITORIES: ENA
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Project description:Banned from mass production, polychlorinated biphenyls (PCBs) still pose a neurological health threat decades later. PCB52, a volatile compound, has been found in the indoor air of schools where adolescent students and staff are exposed. The adolescent brain is vulnerable and highly influenced by the environment around it. This study used adolescent Sprague-Dawley rats to determine the neurological effects of a subacute (28-day) PCB52 inhalation exposure. Rats were exposed 4 h a day for 28 consecutive days with neurobehavioral tests conducted during the last 5 days of exposure. Based on the data including brain weights, PCB52 and metabolite levels, gene expression in the striatum and cerebellum, and neurobehavioral tests (Y-maze, HBT, OFT, and EPM); a subacute inhalation of PCB52 results in sex-specific differences in response to exposure. Our results indicate multilevel PCB52 influence that is different in adolescent males and females; from gene expression to downstream innate mechanisms driving behavior.
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Project description:Polychlorinated biphenyls (PCBs) are persistent environmental toxicants that pose a variety of health risks in humans. PCB 52 has been found in the indoor air of schools where adolescent students and staff are being actively exposed. This study examined the three different fat depots, namely, brown adipose tissue (BAT), subcutaneous adipose tissue (SAT), and visceral adipose tissue (VAT), of adolescent Sprague-Dawley rats after sub-acute exposure to PCB 52 via nose-only inhalation. Rats were exposed for 4 hours daily for 28 consecutive days. RNA extracted from both male and female fat depots were submitted for RNA sequencing to compare the effects of PCB 52 on the expression of genes in the fat depots.
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Project description:In this work we study the pulmonary toxicological properties of titanium dioxyde nanoparticles using molecular toxicological approach. For this, we exposed F344 rats by nose-only inhalation 6 hours/day, 5 days/week for 4 weeks. Lung samples have been collected up to 28 days after the end of exposure and transcriptomics analysis were performed.
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Project description:MicroRNAs (miRNAs) are critical regulators of gene expression, yet much remains unknown regarding miRNA changes resulting from environmental exposures and whether they influence pathway signaling across various tissues and time. To gain knowledge on these novel topics, we set out to investigate in vivo miRNA responses to inhaled formaldehyde, an important air pollutant known to disrupt miRNA expression profiles. Rats were exposed by inhalation to either 0 or 2 ppm formaldehyde (6 hours/day) for 7 days, 28 days, or 28 days followed by a 7 day recovery. Genome-wide miRNA expression profiles and associated signaling pathways were assessed within the nasal respiratory mucosa, circulating mononuclear white blood cells (WBC), and bone marrow (BM). Male Fischer rats received nose-only inhalation exposures of 2 ppm formaldehyde. Three exposure durations were investigated: (1) 2 ppm formaldehyde exposure, 6 hours/day, for 7 days (7-day group), (2) 2 ppm formaldehyde exposure, 6 hours/day, for 28 days (28-day group), and (3) 2 ppm formaldehyde exposure, 6 hours/day, for 28 days, with a 7 day recovery period following the last exposure (28-day plus recovery group). Control (unexposed) rats were placed in nose-only exposure tubes containing room air for the same duration. After the last exposure period (or the last recovery period for the 28-day plus recovery group), animals were euthanized. RNA were assessed from sampes collected from the nasal epithelium, circulating white blood cells, and bone marrow cells. Genome-wide miRNA expression profiles were evaluated using microarrays.
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