Beneficial effects of vitamin C treatment on pregnant rats exposed to formaldehyde: Reversal of immunosuppression in the offspring

Inhalation of formaldehyde (FA) during the pregnancy induces oxidative stress in the uterus, and here we hypothesized that this mechanism may be responsible for the impaired immune response detected in the offspring. In order to investigate the protective effects of Vitamin C on the oxidative stress...

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Veröffentlicht in:Toxicology and applied pharmacology 2016-06, Vol.300, p.77-81
Hauptverfasser: Ibrahim, Beatriz Silva, Barioni, Éric Diego, Heluany, Cíntia, Braga, Tárcio Teodoro, Drewes, Carine Cristiane, Costa, Silvia Goes, Câmara, Niels Olsen Saraiva, Farsky, Sandra Helena Poliselli, Lino-dos-Santos-Franco, Adriana
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Sprache:eng
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Zusammenfassung:Inhalation of formaldehyde (FA) during the pregnancy induces oxidative stress in the uterus, and here we hypothesized that this mechanism may be responsible for the impaired immune response detected in the offspring. In order to investigate the protective effects of Vitamin C on the oxidative stress induced by FA in the uterine microenvironment, pregnant Wistar rats were treated with vitamin C (150mg/kg, gavage) or vehicle (distilled water, gavage) 1h before FA exposure (0.92mg/m3, 1h/day, 5days/week), for 21days, and the 30days old offspring were submitted to LPS injection (Salmonella abortus equi, 5mg/kg, i.p.). The enhanced gene expression of iNOS, COX-1 and COX-2 and decreased gene expression of SOD-2 in the uterus of FA exposed mothers was rescued by Vit C treatment. Moreover, vitamin C rescued the impaired immune response elicited by LPS in the offspring from FA exposed mothers, by increasing the number of blood and bone marrow leukocytes, and augmenting gene expression of IL-6 and reducing mRNA levels of IL-10 and IFN in the lungs. Vitamin C treatment did not rescue the impaired TLR4-NF-kB pathway in the lung of the offspring, suggesting that FA-induced uterine oxidative stress affects other inflammatory pathways activated by LPS in the offspring. Together, data obtained here confirm our hypothesis that FA-induced oxidative stress in the uterine microenvironment modifies the programming mechanisms of the immune defenses of offspring, leading to an impaired host defense. •FA exposure during pregnancy induces oxidative stress in the uterus.•Vitamin C treatment blunted the oxidative stress in uterus induced by FA exposure.•Oxidative stress in uterus after FA exposure impairs the immune response of offspring.•Vitamin C in pregnant rats rescued the impaired immune response in the offspring.
ISSN:0041-008X
1096-0333
DOI:10.1016/j.taap.2016.03.010