L-ascorbic acid can be pro-oxidant and anti-oxidant in different reaction. This study aims to test the effects about products of oxidized L-Ascorbic Acid on acellular DNA.

Purpose: To study the health effects of coal mine environment on workers, to discover early effective biomarkers. Methods: A cross-sectional survey was conducted with 502 in-service workers, and the population was divided into the coal miner and the auxiliary worker. Clinical examinations were carried out by qualified doctors. Peripheral blood was collected to measure blood biochemistry, hemogram and karyotype apoptosis. Results: All workers were healthy and showed no difference in age, height, weight and BMI between groups. The education level and working years of coal miners were significantly lower than that of auxiliary workers (P < 0.05). Compared with auxiliary workers, the concentration and percentage of LYMPH, BASO, EO, RBC and the concentration of HGB of coal miners decreased (P < 0.05). The percentage of NEUT of coal miners increased (P < 0.05). The coal miner presented higher BUN, lower CRE, and higher BUN/CRE (P < 0.05). The proportion of karyotype apoptosis of coal miners was higher (P < 0.05). Conclusions: The coal mine environment impacts immune system, induces adverse effects on renal function and enhances the risk of anemia of coal miners. And karyotype apoptosis, LYMPH, BUN/CRE and HGB can be used as early effective biomarkers for coal miners.

Background: Natural differences in running capacities among rats remain poorly understood, and the mechanisms driving these differences need further investigation. Methods: Twenty male Sprague-Dawley (SD) rats were selected. High and low running capacity rats were identified using Treadmill Exhaustion Tests. Peripheral blood was collected for serum isolation, followed by metabolomics analysis using LC-MS/MS. Data were preprocessed, and principal component analysis (PCA) and partial least squares-discriminant analysis (PLS-DA) were applied to identify metabolic profile differences. Significant metabolites were screened, and pathway enrichment analysis was conducted using the KEGG database to determine key metabolic pathways. Forty SD rats (equal male and female) were randomly divided into an ITP group (24.29 mg/kg.bw) and a control group. Running capacity was assessed after one week of continuous treatment. Results: Three independent measurements showed consistent differences in running capacity. A total of 519 differential metabolites were identified, with 255 up-regulated and 264 down-regulated. KEGG pathway analysis revealed significant enrichment of the Purine Metabolism pathway (ITP-ATP ) in the high running capacity group (P< 0.05). The ITP-treated group exhibited significantly higher running capacity than controls (P< 0.05), confirming the efficacy of dietary ITP supplementation. Conclusion: The running capacity of rats is influenced by the ITP-ATP pathway,and exogenous ITP administration through dietary intervention significantly improves running ability.

Caffeine is among the world's most widely consumed psychoactive substances, yet its potential to interact with the endocrine system, particularly as an estrogen mimic, remains ambiguous and inadequately characterized using validated in vivo models. Our objective is to definitively assess the intrinsic estrogenic activity of caffeine and its potential interaction with a reference estrogen using the standardized OECD 440 uterotrophic bioassay. Immature female Sprague-Dawley rats (n = 10/group) were administered vehicle, caffeine (10, 20, or 40 mg/kg/day), 17β-estradiol (positive control), or estradiol combined with caffeine for three consecutive days. Uterine wet and blotted weights were measured 24 h post-final dose, and the uterotrophic response was evaluated. As expected, estradiol treatment provoked a robust uterotrophic response, increasing uterine wet weight over 4-fold and blotted weight over 3.7-fold compared to controls (P < 0.001). In contrast, caffeine alone at all tested doses failed to produce any significant increase in uterine weight, indicating a lack of intrinsic estrogenic activity. Notably, co-administration of caffeine with estradiol significantly attenuated the estradiol-induced response, reducing wet weight by approximately 33% and blotted weight by 25% (P < 0.05). These findings demonstrate that caffeine is not an estrogen agonist in this validated in vivo model. Co-administration with estradiol significantly reduced the uterotrophic response, suggesting a potential interaction that warrants further mechanistic investigation.