Microplastic (MPs) pollution is widespread in the environment and poses growing risks to food safety and human health. In a 60-day oral exposure study, male Swiss mice received MPs (10 mg/kg b.wt), an Show more
Microplastic (MPs) pollution is widespread in the environment and poses growing risks to food safety and human health. In a 60-day oral exposure study, male Swiss mice received MPs (10 mg/kg b.wt), and the neuroprotective potential of taurine (Tau, 200 mg/kg b.wt) was evaluated. MPs exposure induced pronounced anxiety-like behavior, evidenced by increased peripheral zone activity in the open field test (+ 81.1%) and elevated anxiety index in the elevated plus maze (+ 75.9%), along with significant memory and spatial learning impairments in the Y-maze (increased trials + 31.6% and latency + 75.2%). Neurochemically, MPs increased acetylcholinesterase (AChE) activity (+ 89.4%) while reducing dopamine (-29.4%) and γ-aminobutyric acid (GABA) (-17.9%) levels. MPs also triggered marked oxidative stress, as shown by elevated reactive oxygen species (+ 107.6%) and malondialdehyde (+ 249.0%), accompanied by reduced total antioxidant capacity (-26.2%). At the molecular level, MPs downregulated CREB1 (-82.2%) and BDNF (-80.2%) while markedly upregulating AKT1 (~ fivefold) and pro-inflammatory cytokines (TNF-α, IL-6, CXCL-10, and IL-1β; 5.2-7.2-fold). Histopathological analysis revealed severe neurodegenerative alterations across the cerebrum, hippocampus, and cerebellum. Tau co-treatment significantly ameliorated MPs' induced neurotoxicity by reducing anxiety and memory deficits, lowering AChE activity (- 17.3%), restoring dopamine (+ 28.8%) and GABA (+ 14.2%) levels, attenuating oxidative stress (ROS -45.4% and MDA -44.7%), suppressing inflammatory gene expression (-51.0 to -68.1%), and partially normalizing CREB1 and BDNF expression (+239% and +240%, respectively). Collectively, these findings identify Tau as a promising natural neuroprotective agent against MPs' induced neurotoxicity. Show less
End-stage kidney disease (ESRD) patients on dialysis face pronounced cardiovascular and metabolic risks due to disruptions in lipoprotein(a), phosphorus, potassium, uric acid, and lipid balance. Curre Show more
End-stage kidney disease (ESRD) patients on dialysis face pronounced cardiovascular and metabolic risks due to disruptions in lipoprotein(a), phosphorus, potassium, uric acid, and lipid balance. Current therapeutic options offer limited capacity to address these multifaceted abnormalities. Niacin is unique in this regard, as it not only lowers lipoprotein(a) but also influences phosphorus and uric acid metabolism. This study evaluates the efficacy of niacin therapy in improving these biochemical markers, thereby addressing an important therapeutic gap in this vulnerable population. In a randomized, controlled trial, 50 hemodialysis patients were divided into two groups of twenty-five each. The control group continued standard care, while the niacin group received 500 mg/day niacin alongside standard therapy. Patients were followed for 3 months. Systolic and diastolic blood pressure were stabilized by niacin administration, in contrast to the control group, where both parameters rose significantly. Phosphorus decreased significantly in the niacin group (5.59 to 4.85 mg/dL, Niacin (500 mg/day) offers significant cardiovascular and metabolic benefits for hemodialysis patients, supporting its role as an adjunctive therapy in managing ESRD-associated risks. https://clinicaltrials.gov/, NCT06406140. Show less