Ascorbic acid is a water-soluble chain breaking antioxidant. It scavenges free radicals and reactive oxygen species (ROS), which are produced during metabolic pathways. Exercise can produce an imbalance between ROS and antioxidants, leading to oxidative stress-related tissue damages. This study was designed to determine the effects of ascorbic acid supplementation on circulating biomarkers of oxidative stress and muscle damage following a single bout of exercise. In a crossover design with a 1 wk. wash-out period, 19 healthy women performed 30 min moderate-intensity cycling after ingesting 1000 mg of ascorbic acid (AA) or placebo. Blood samples were taken immediately before, immediately after and 30 min post-exercise to determine plasma albumin, total protein, glucose, oxidative stress and muscle damage markers. Plasma albumin and total protein levels increased immediately after exercise in placebo alongside slight reductions in glucose (p = 0.001). These effects were absent in AA cohort. Ferric reducing ability of plasma and vitamin C levels in AA cohort significantly increased after exercise (p < 0.05). Superoxide dismutase activity was significantly elevated after exercise (p = 0.002) in placebo but not AA. Plasma malondialdehyde did not change after exercise in placebo but was significantly decreased in AA (p < 0.05). The exercise protocol promoted slight muscle damage, reflected in significant increases in total creatine kinase in all subjects after exercise. On the other hand, plasma C-reactive protein and lactate dehydrogenase remained unchanged. Supplementation with ascorbic acid prior exercise improves antioxidant power but does not prevent muscle damage.

The purpose of this study was to investigate the impact of ascorbic acid (AA) consumption on the oxidative stress status of untrained volunteers participating in a supervised exercise program. The study included 46 young adults (average age, 23.5 ± 0.59 years; 37 females, 9 males) who remained sedentary (n = 16) or participated in 30 min of outdoor aerobic running (n = 30) at an intensity corresponding to 65%–75% of maximum heart rate for 3 times per week for 12 weeks. Exercised subjects were randomly assigned to an exercise group without AA supplementation (control; n = 10) or received either 250 mg (n = 10) or 500 mg (n = 10) of AA supplementation previous to each exercise session. Blood samples were taken on day 0 and day 84 to evaluate metabolic profiles and antioxidant status. Sedentary subjects underwent in a single bout of aerobic running to determine total antioxidant status (TAS) and malondiadehyde (MDA) at pre- and postexercise with or without AA supplementation. No significant change in TAS was observed. Plasma MDA significantly increased at postexercise (P < 0.05), and AA supplementation decreased MDA level significantly (P < 0.05). After 3 months of exercise, there was no significant change in blood glucose, lipid profile, MDA, TAS, superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase activities amongst groups. Supplementation of AA was associated with minor and inconsistent reductions in SOD, GPx, and catalase activities (P < 0.05). These findings indicate that pre-exercise supplementation of ascorbic acid does not alter oxidative stress markers in the plasma and erythrocytes of young adults engaged in a supervised exercise program.

Background: The urinary albumin–to–creatinine ratio (UACR) is a key marker for early kidney dysfunction. This study assessed UACR levels and their associations with demographic and clinical factors in a Thai university population. Materials and methods: A cohort of 158 participants (53 males, 105 females) was recruited from Chiang Mai University between January and May 2024. Urinary albumin and creatinine were measured by turbidimetric immunoassay and creatininase method, respectively, and expressed as UACR (mg/gm creatinine). UACR was categorized as normoalbuminuria (0.05), whereas obesity class II, elevated fasting blood glucose (≥126 mg/dL) and systemic lupus erythematosus (SLE) were significantly associated with increased urinary albumin excretion (Chi-square, p<0.05). Conclusion: Elevated blood glucose, obesity, and SLE were significantly linked to increased UACR, emphasizing the importance of early identification and management of these risk factors to prevent kidney disease progression.

Glucosidase II (GluII) is a heterodimeric enzyme localized in the endoplasmic reticulum (ER), essential for the sequential trimming of glucose residues during N-linked glycosylation. This critical function facilitates glycoprotein folding via the calnexin/calreticulin chaperone system, maintaining ER homeostasis. Dysregulation or inhibition of GluII has been implicated in various pathological processes, including cancer, viral infections, and glycoprotein misfolding disorders. This review summarizes the current knowledge of GluII’s structure and function, highlights a wide range of natural and synthetic GluII inhibitors—including iminosugar derivatives (e.g., deoxynojirimycin (DNJ), castanospermine (CAST)), non-iminosugar compounds (e.g., bromoconduritol, catechins), and mechanism-based cyclophellitol analogues—and evaluates their biological effects and therapeutic potential. The cellular impact of GluII inhibition is explored in the context of ER stress, unfolded protein response (UPR), tumor cell apoptosis, and viral replication. Key challenges in developing selective GluII inhibitors are discussed, with a focus on strategies to minimize off-target effects, including prodrug design, allosteric modulation, and emerging genetic approaches such as microRNA (miRNA)-mediated downregulation of GluII subunits. Taken together, these insights underscore the therapeutic relevance of GluII as a druggable target and pave the way for the rational design of next-generation inhibitors in oncology, infectious diseases, and metabolic disorders.

Background/Objective: Albuminuria is an early marker of kidney damage and cardiovascular risk. However, data on its prevalence and association with urine dipstick parameters in heterogeneous, hospital-based populations remain limited. The objective of this study was to determine the prevalence of elevated albuminuria measured by the urine albumin-to-creatinine ratio (UACR) in a diverse patient population and evaluate associations with semi-quantitative urine dipstick parameters. Methods: This cross-sectional study included 393 adults recruited from a tertiary-care hospital setting, comprising individuals undergoing clinical evaluation and routine health assessments. Given the hospital-based recruitment and enrichment with chronic conditions, the study population represents a high-risk cohort rather than the general population. Spot urine samples were analyzed for the UACR and dipstick parameters. Elevated albuminuria was defined as a UACR ≥ 30 mg/g. Associations were assessed using chi-square tests and multivariate logistic regression, with adjusted odds ratios (aORs) and 95% confidence intervals (CIs). Results: Elevated albuminuria was observed in 64% of participants. This high prevalence likely reflects the underlying clinical characteristics of the study population, including a substantial burden of chronic kidney disease and other comorbidities, and should not be interpreted as representative of population-level prevalence. Chronic kidney disease was independently associated with elevated albuminuria (aOR 3.14, 95% CI 1.12–8.86, p = 0.030), as was male sex (aOR 1.54, 95% CI 1.01–2.34, p = 0.045). Dipstick-positive blood was significantly associated with elevated albuminuria (85% vs. 60% in those without dipstick blood positivity, p = 0.005). Dipstick albumin strongly correlated with the UACR (p < 0.001), although 22% of individuals with negative dipstick albumin still had an elevated UACR. Other urine dipstick parameters were not significantly associated with elevated albuminuria. Conclusions: In this high-risk, hospital-based cohort, elevated albuminuria was common and associated with kidney disease and male sex. Dipstick blood positivity is significantly associated with albuminuria and may warrant further investigation. However, reliance on dipstick testing alone may underestimate disease burden, supporting the need for broader implementation of UACR-based screening strategies.