Search

In this study, we seek to determine the association between the polymorphism of the ADIPOQ (rs1501299) gene and adiponectin levels in gestational diabetes mellitus (GDM) patients.

Doxorubicin (DOX) is a chemotherapeutic agent and is widely used in cancer treatment. There are some studies suggesting oxidative stress-induced toxic changes in the liver due to DOX administration. The aim of this study was to reveal the oxidative damage of DOX in liver tissue at molecular level and to evaluate the protective effect of N-acetyl cysteine (NAC) against DOX oxidative damage. Twenty four rats weighing 150-200 g were randomly divided into four equal groups; group 1: control, group 2: received a single dose of DOX, group 3: received NAC for 28 days and group 4: received a single dose of DOX, followed by NAC for 28 days. At the end of the experiment, liver tissues were taken from all animals. Total Antioxidant Capacity (TAC), Total Oxidant Capacity (TOC) levels were determined in these samples by spectrophotometric methods. The histopathological changes of liver tissue were observed routinely in histological staining. It was determined that TOC level increased, TAC levels decreased in the group given DOX compared to the control group. In addition, TAC levels increased in the DOX+NAC group. It was showed the occurrence of congestion in portal triad, and pycnotic cells degeneration in DOX group. It was concluded that DOX administration increased oxidative stress and NAC administration could prevent the increased oxidative stress (p<0.05). NAC caused modulatory effects on oxidative stress and antioxidant redox system in DOXinduced liver toxicity in the rat. [ABSTRACT FROM AUTHOR]

Objective: Cadmium (Cd) is a well-known widespread environmental pollutant and is not rapidly excreted by the kidneys; instead, it accumulates and causes kidney damage. This study aimed to compare the effects of antioxidant curcumin and resveratrol on antioxidant defense in Cd-induced rat kidney tissue. Methods: In the study, 36 (200-250 gr) Wistar albino rats were divided into 6 (n=6) groups. Group 1: control; group 2: CdCl2; group 3: curcumin; group 4: CdCl2 + curcumin; group 5: resveratrol; group 6: CdCl2 + resveratrol. At the end of the experiment, malondialdehyde (MDA), total oxidant capacity (TOC), and total antioxidant capacity (TAC) activities were measured in kidney tissues. Results: In the CdCl2-treated group, oxidative stress index (OSI), TOC, and MDA levels increased compared with the control group, and TAC values decreased (p<0.05). In the case of resveratrol or curcumin administered with Cd, TAC levels increased, MDA levels, and OSI values decreased compared with the group administered only Cd (p<0.05). Conclusion: Both resveratrol and curcumin may have protective effects in the kidneys against CdCl2-induced oxidative damage. [ABSTRACT FROM AUTHOR]

Several studies have reported differences in radiation toxicity between the sexes, but these differences have not been tested with respect to histopathology and genes. This animal study aimed to show an association between histopathological findings of radiation-induced lung toxicity and the genes ATM, SOD2, TGF-β1, XRCC1, XRCC3 and HHR2. In all, 120 animals were randomly divided into 2 control groups (male and female) and experimental groups comprising fifteen rats stratified by sex, radiotherapy (0 Gy vs. 10 Gy), and time to sacrifice (6, 12, and 24 weeks postirradiation). Histopathological evaluations for lung injury, namely, intra-alveolar edema, alveolar neutrophils, intra-alveolar erythrocytes, activated macrophages, intra-alveolar fibrosis, hyaline arteriosclerosis, and collapse were performed under a light microscope using a grid system; the evaluations were semi quantitatively scored. Then, the alveolar wall thickness was measured. Real-time quantitative reverse transcription PCR (RT-qPCR) was used to determine gene expression differences in ATM, TGF-β1, XRCC1, XRCC3, SOD2 and HHR2L among the groups. Histopathological data showed that radiation-induced acute, subacute, and chronic lung toxicity were worse in male rats. The expression levels of the evaluated genes were significantly higher in females than males in the control group, but this difference was lost over time after radiotherapy. Less toxicity in females may be attributable to the fact that the expression of the evaluated genes was higher in normal lung tissue in females than in males and the changes in gene expression patterns in the postradiotherapy period played a protective role in females. Additional data related to pulmonary function, lung weights, imaging, or outcomes are needed to support this data that is based on histopathology alone. [ABSTRACT FROM AUTHOR]