کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5846180 1128457 2014 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Exposure to low doses of formaldehyde during pregnancy suppresses the development of allergic lung inflammation in offspring
ترجمه فارسی عنوان
قرار گرفتن در معرض دوزهای کم فرمالدئید در دوران بارداری باعث کاهش التهاب آلرژیک در فرزندان می شود
کلمات کلیدی
آلاینده ها، آسم، سیتوکین ها، سنتز آنتیبادیهای آنافیلاکتیک، مکانیسم برنامه ریزی، استرس اکسیداتیو،
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم محیط زیست بهداشت، سم شناسی و جهش زایی
چکیده انگلیسی


- Formaldehyde exposure does not cause lung inflammation in pregnant rats.
- Formaldehyde exposure suppresses allergic lung inflammation in the offspring.
- Formaldehyde exposure induces oxidative stress in uterine environment.

Formaldehyde (FA) is an environmental and occupational pollutant, and its toxic effects on the immune system have been shown. Nevertheless, no data are available regarding the programming mechanisms after FA exposure and its repercussions for the immune systems of offspring. In this study, our objective was to investigate the effects of low-dose exposure of FA on pregnant rats and its repercussion for the development of allergic lung inflammation in offspring.Pregnant Wistar rats were assigned in 3 groups: P (rats exposed to FA (0.75 ppm, 1 h/day, 5 days/week, for 21 days)), C (rats exposed to vehicle of FA (distillated water)) and B (rats non-manipulated). After 30 days of age, the offspring was sensitised with ovalbumin (OVA)-alum and challenged with aerosolized OVA (1%, 15 min, 3 days). After 24 h the OVA challenge the parameters were evaluated.Our data showed that low-dose exposure to FA during pregnancy induced low birth weight and suppressed the development of allergic lung inflammation and tracheal hyperresponsiveness in offspring by mechanisms mediated by reduced anaphylactic antibodies synthesis, IL-6 and TNF-alpha secretion. Elevated levels of IL-10 were found. Any systemic alteration was detected in the exposed pregnant rats, although oxidative stress in the uterine environment was evident at the moment of the delivery based on elevated COX-1 expression and reduced cNOS and SOD-2 in the uterus. Therefore, we show the putative programming mechanisms induced by FA on the immune system for the first time and the mechanisms involved may be related to oxidative stress in the foetal microenvironment.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology and Applied Pharmacology - Volume 278, Issue 3, 1 August 2014, Pages 266-274
نویسندگان
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