ObjectiveThis study was designed to investigate the effect of nicotine on serum
progesterone and estradiol levels as possible cause of abortion during first
trimester of gestation in female Wistar rats.MethodsFourteen female rats with regular estrous cycles in the same phase of cycle
were divided into two groups (Control and Nicotine-treated) with each group
receiving 1ml of distilled water and 1mg/kg of nicotine respectively for the
first seven days of pregnancy (GD1-7). The animals were sacrificed on the
8th day and blood samples were collected for hormonal
analyses. Ovaries and uteruses were excised, weighed, and prepared for
histological study.ResultsThis study revealed a significant decrease in serum progesterone and
estradiol levels in the nicotine-treated group when compared to controls.
The histological findings equally showed degeneration in the
cytoarchitecture of the ovary of the nicotine-treated group.ConclusionThe observed hormonal imbalances and alteration in the cytoarchitecture of
the ovary caused by nicotine in the first trimester of pregnancy may result
in abortion during this period.
Background
Oxidative damage is critical in the pathogenesis of ovarian ischaemia/reperfusion (I/R) injury, and statins have been reported to exert antioxidant activity. However, the role of VCAM-1 and xanthine oxidase (XO)/uric acid (UA) in ovarian I/R injury is not known. Also, whether or not atorvastatin exerts antioxidant activity like other statins is unclear.
Objectives
This study investigated the involvement of VCAM-1 and XO/UA in ovarian I/R injury and the likely protective role of atorvastatin.
Methods
Forty female Wistar rats were randomized into sham-operated, ischaemia, ischaemia/reperfusion (I/R), ischaemia and atorvastatin, and I/R and atorvastatin.
Results
In comparison with the sham-operated group, atorvastatin blunted ischaemia and I/R-induced distortion of ovarian histoarchitecture and follicular degeneration. Also, atorvastatin alleviated ischaemia and I/R-induced rise in XO, UA, and malondialdehyde, which was accompanied by inhibition of ischaemia and I/R-induced reductions in reduced glutathione level, enzymatic antioxidant activities and increase in myeloperoxidase activity and TNF-α and IL-6 levels by atorvastatin treatment. Additionally, atorvastatin blocked ischaemia and I/R-induced increase in VCAM-1 expression, caspase 3 activity, 8-hydroxydeoxyguanosine level and ovarian DNA fragmentation index.
Conclusion
For the first time, this study revealed that atorvastatin-mediated downregulation of VCAM-1 and XO/UA/caspase 3 signaling averts oxidative injury, inflammation, and apoptosis induced by ovarian ischaemia/reperfusion injury.
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