OXIDATIVE STRESS MARKERS

The global consumption of energy drinks and caffeine-containing beverages has increased due to their stimulating effects, yet concerns regarding their impact on oxidative stress remain largely unaddressed. This study investigates the effects of energy drinks and caffeine on oxidative stress markers, including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and malondialdehyde (MDA), in heart and kidney tissues. Fifty (50) young Sprague-rats weighing between 164g-250g were used for this study. The rats were divided into five groups; Group 1 as control (n=10) received water, Group 2 (n=10) received 5ml of energy drink, Group 3 (n=10) received 10ml energy drink, Group 4 (n=10) received 5ml of caffeine 0.89mg/kg b.w., Group 5 (n=10) received 10ml of caffeine 2.0mg/kg b.w. The various doses of energy drinks and caffeine were administered orally daily for six weeks .Weight of rats were taken weekly, at the end of the experimental period, the rats were sacrificed and organs collected into plain tubes filled with normal saline solution. Oxidative stress parameters were measured using spectrophometric method. Results were presented as standard error of mean (SEM). Analysis of variance (ANOVA) was used to compare the means of tests and control value while the post-hoc test was done using Dunnett’s multiple comparison tests and a p-value of less than 0.05 was considered statistically significant. Results showed that energy drinks increased antioxidant enzyme activities in the heart but also elevated MDA levels, indicating oxidative stress. Caffeine reduced antioxidant activity in the heart and increased MDA levels in the kidney, signifying oxidative damage. These effects were tissue-specific and dose-dependent, highlighting potential health risks. In conclusion, excessive consumption of energy drinks and caffeine may pose health risks due to oxidative stress. Therefore, public awareness and regulatory measures are essential to mitigate these effects.

Bisphenol-A (BPA) is an industrial chemical primarily used in the production of polycarbonate plastics and epoxy resins. Selenium (Se) is an essential trace element, vital for the health of humans and other living organisms. The aim of this study was to investigate the effects of Bisphenol-A (BPA) on some oxidative stress markers in adult male rats and evaluate the potential effect of Selenium (Se) in BPA-induced oxidative damage. A total of twenty (20) male Wistar rats weighing between 180g and 200g were purchased and kept in standard cages for two weeks to enable them acclimatize to their new environment. After acclimatization period, the twenty-adult male Wistar rats were divided into four (4) different groups A, B, C, D: control, BPA-only, Se-only, and BPA+Se. Group A served as control, Groups B D received 20mg/kg BPA, 2mg/kg Se, and both, respectively, for 54 days. Blood was collected and analyzed for oxidative stress parameters such as malondialdehyde (MDA), superoxide Distumates (SOD) and catalase (CAT). All statistical analyses were carried out using Graph Pad prism statistical software version 10.0. The data from all the groups were presented as Mean ± S.E.M (Standard Error of Mean), (n=5) in each group and analyze for statistical significance using one-way Analysis of Variance (ANOVA). Values were considered significant at P<0.05. The result shows that exposure to BPA resulted in significant (p<0.05) reduction in body weight. There was significant (p<0.05) increase in MDA levels in all groups compared with the control. On the other hand, SOD and CAT activities were significantly (p<0.05) reduced in all groups compared with the control, thereby indicating decreased antioxidant enzyme activities. In conclusion, these finding shows that Selenium (Se) supplementation did not mitigate the adverse effects of BPA and instead worsened oxidative stress, implying that Selenium (Se) may not provide protection against the harmful effect of Bisphenol-A (BPA) even at this dose but rather potentiated the effect of Bisphenol-A (BPA).