Abstract. MicroRNAs (miRNAs) are small non-coding RNAs that function as crucial regulators of gene expression. Recently, dysregulation of miRNA expression in the blood has been demonstrated to be associated with various diseases, including type 2 diabetes mellitus (T2D), suggesting a potential for their use as biomarkers of disease prognosis. The present study examined the expression levels of T2D-associated miR-15a in peripheral whole blood samples from patients with T2D, pre-diabetes individuals exhibiting impaired fasting glucose (IFG) and impaired glucose tolerance (IGT), as well as healthy control subjects, in order to investigate the potential of peripheral blood miR-15a as a biomarker for the prediction of T2D and pre-diabetes. The present study included 24 patients with T2D, 22 IFG/IGT individuals and 24 healthy controls. The expression levels of miR-15a were analyzed by reverse transcription-quantitative polymerase chain reaction. The results indicated that the peripheral blood miR-15a expression levels were significantly decreased in patients with T2D and IFG/IGT individuals, compared with healthy control subjects (P<0.05). As determined by multivariate logistic regression analysis, lower miR-15a expression was significantly associated with T2D (odds ratio [OR], 0.51; 95% confidence interval [CI], 0.16-0.73; P<0.05) and pre-diabetes (OR, 0.56; 95% CI, 0.23-0.79; P<0.05). This association remained statistically significant following adjustment for age, body mass index and hypertension, as well as other biochemical indicators. Furthermore, a receiver operating characteristic analysis revealed that blood miR-15a distinguished patients with T2Dand IFG/IGT individuals from healthy controls (area under the curves; 95% CI: 0.864; 0.751-0.977 and 95% CI: 0.852; 0.752-0.953, respectively). These results demonstrated that peripheral blood miR-15a expression levels were significantly lower in patients with T2D and IFG/IGT individuals, compared with healthy individuals. Thus, miR-15a in peripheral whole blood may serve as a potential biomarker for T2D and pre-diabetes.

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Acetochlor is persistently used in the agroproduction sector to control broadleaf weeds. Due to frequent and continuous applications, this herbicide can reach nearby water bodies and may induce deleterious changes in aquatic life. Therefore, investigation of harmful impacts of different environmental pollutants, including herbicides, is vital to knowing the mechanisms of toxicity and devising control strategies. The current experiment included bighead carp ( n = 80 ) to estimate adverse impacts. Fish were randomly placed in 4 different experimental groups (T0-T3) and were treated for 36 days with acetochlor at 0, 300, 400, and 500 μg/L. Fresh blood without any anticoagulant was obtained and processed for nuclear and morphological changes in erythrocytes. At the same time, various visceral organs, including the gills, liver, brain, and kidneys, were removed and processed on days 12, 24, and 36 to determine oxidative stress and various antioxidant biomarkers. Comet assays revealed significantly increased DNA damage in isolated cells of the liver, kidneys, brain, and gills of treated fish. We recorded increased morphological and nuclear changes ( P ≤ 0.05 ) in the erythrocyte of treated fish. The results on oxidative stress showed a higher quantity of oxidative biomarkers and a significantly ( P ≤ 0.05 ) low concentration of cellular proteins in the gills, liver, brain, and kidneys of treated fish compared to unexposed fish. Our research findings concluded that acetochlor renders oxidative stress in bighead carp.

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