Consumption of High Salt-Diet Causes Cortical and Hippocampal Lipid Peroxidation via Endogenous Antioxidant Depletion in Sleep Deprived Adult Female Wistar Rats

Abstract

Excessive dietary salt intake is a major global health concern, particularly in low- and middle-income countries, where it significantly contributes to hypertension and other non-communicable diseases. Concurrently, chronic sleep deprivation is increasingly recognized as an independent risk factor for neurological and cardiovascular dysfunction. While each stressor individually impairs health, its combined impact on hippocampal oxidative balance and cognition remains poorly understood. In this study, twenty Adults female Wistar rats weighing 120-150 g were randomly assigned into four groups (n = 5 per group): control, high-salt diet (5% NaCl supplementation), sleep-deprived, and combined high-salt plus sleep-deprived. At the end of the experimental period, hippocampal tissue and blood samples were analyzed for oxidative stress biomarkers, including malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH). Cognitive performance was assessed using hippocampal-sensitive antioxidant assays. The combined high-salt and sleep-deprived group exhibited pronounced elevations in hippocampal and brain MDA levels (514.70 ± 10.03 vs. 436.32 ± 8.39) alongside significant reductions in CAT (3.60 ± 0.48 vs. 2.68 ± 0.19) and SOD (5.08 ± 0.45) activity compared to controls. These alterations were associated with impaired spatial learning and memory, consistent with hippocampal oxidative stress. Our findings demonstrate that concurrent high-salt intake and sleep deprivation synergistically disrupt hippocampal redox homeostasis and impair cognitive outcomes in female Wistar rats. This highlights the compounded risk posed by poor dietary patterns and inadequate sleep, with important implications for populations experiencing overlapping nutritional and lifestyle stressors.