ascorbic-acid and Uterine-Diseases

To investigate the effectiveness of intraperitoneal vitamin C (VC) and vitamin E (VE) in the prevention of postoperative adhesion formation in a rat uterine horn model.. Twenty-eight Wistar albino rats were divided into four groups in which: control group, the abdomen was opened and closed without any intervention; adhesion group, a 2-cm linear incision was performed on the uterine horn and closed; VC group, VC was administrated i.p., and 15 min later a 2-cm incision was performed on the uterine horn and closed; and VE group, VE was administrated i.p., and 15 min later a 2-cm incision was performed on the uterine horn and closed. Re-laparotomy was performed 15 days later. Right uterine horn adhesions were evaluated according to macromorphological characteristics and tissue sections were further examined for fibrosis, angiogenesis and vascular endothelial growth factor (VEGF), type I collagen and malondialdehyde (MDA) scoring. Kruskal-Wallis anova and Mann-Whitney U-test were utilized for statistical analysis.. Adhesion area and also strength were significantly lower in the VC group and the VE group compared with the adhesion group. Fibrosis and angiogenesis scores were observed to be significantly higher in the adhesion group compared with the VC group and the VE group. MDA and VEGF immunoreactivity were also found to be significantly lower in the VC group and the VE group compared with the adhesion group. However, there was no significant difference between the VC group and the VE group with respect to all the above parameters.. Administration of VC or VE i.p. was observed to be effective in the prevention of postoperative adhesion formation in an experimental model.

Topics: Animals; Antioxidants; Ascorbic Acid; Female; Injections, Intraperitoneal; Postoperative Complications; Rats; Rats, Wistar; Tissue Adhesions; Uterine Diseases; Uterus; Vitamin E

There are numerous reports on the effects of electromagnetic radiation (EMR) in various cellular systems. Mechanisms of adverse effects of EMR indicate that reactive oxygen species (ROS) may play a role in the biological effects of this radiation. The aims of this study were to examine 900 MHz mobile phone-induced oxidative stress that promotes production of ROS and to investigate the role of vitamins E and C, which have antioxidant properties, on endometrial tissue against possible 900 MHz mobile phone-induced endometrial impairment in rats. The animals were randomly grouped (eight each) as follows: 1) Control group (without stress and EMR, Group I), 2) sham-operated rats stayed without exposure to EMR (exposure device off, Group II), 3) rats exposed to 900 MHz EMR (EMR group, Group III) and 4) a 900 MHz EMR exposed + vitamin-treated group (EMR + Vit group, Group IV). A 900 MHz EMR was applied to EMR and EMR + Vit group 30 min/day, for 30 days using an experimental exposure device. Endometrial levels of nitric oxide (NO, an oxidant product) and malondialdehyde (MDA, an index of lipid peroxidation), increased in EMR exposed rats while the combined vitamins E and C caused a significant reduction in the levels of NO and MDA. Likewise, endometrial superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities decreased in EMR exposed animals while vitamins E and C caused a significant increase in the activities of these antioxidant enzymes. In the EMR group histopathologic changes in endometrium, diffuse and severe apoptosis was present in the endometrial surface epithelial and glandular cells and the stromal cells. Diffuse eosinophilic leucocyte and lymphocyte infiltration were observed in the endometrial stroma whereas the combination of vitamins E and C caused a significant decrease in these effects of EMR. It is concluded that oxidative endometrial damage plays an important role in the 900 MHz mobile phone-induced endometrial impairment and the modulation of oxidative stress with vitamins E and C reduces the 900 MHz mobile phone-induced endometrial damage both at biochemical and histological levels.

Topics: Animals; Antioxidants; Ascorbic Acid; Cell Phone; Endometrium; Environmental Exposure; Female; Microwaves; Oxidative Stress; Radiation Injuries, Experimental; Rats; Rats, Wistar; Reactive Oxygen Species; Uterine Diseases; Vitamin E

The influence of maternal vitamin C deficiency on fetal development was studied in swine with a hereditary lack of ability to synthesize ascorbic acid (OD pigs). Thirteen pregnant sows homozygous (od/od) for the defect were depleted of ascorbic acid for 24 to 38 d at various stages of gestation. Six normal (OD/OD) sows were used as controls. Only a few experimental sows showed clinical symptoms of vitamin C deficiency. Nevertheless, severe pathological changes were seen in the uterus and fetuses. Characteristic findings were hemorrhages and hematomas in both fetal and maternal placenta, and general edema and subcutaneous hemorrhages in the fetuses. Similarities were noted to the abruptio placentae syndrome in women. Depletion of vitamin C resulted in a pronounced decline in ascorbic acid concentration in most maternal and fetal organs as well as in plasma and embryonic fluids. No morphological malformations were found in the fetuses, but the ossification of the skeleton was severely deranged. Macroscopically the lesions comprised swelling of the costochondral junction and separation of the epiphysial cartilage from the spongiosa in ribs and limb bones. Another characteristic finding was loosening of the periost from the cortex, often resulting in subperiosteal bleedings. Microscopically normal osteoblasts were few and the formation of osteoid defective.

Topics: Animals; Ascorbic Acid; Ascorbic Acid Deficiency; Bone and Bones; Edema; Embryonic and Fetal Development; Female; Fetal Diseases; Fetus; Hematoma; Hemorrhage; Male; Placenta; Placenta Diseases; Pregnancy; Pregnancy Complications; Swine; Swine Diseases; Uterine Diseases; Uterus