Glutathione mitigates hippocampal aluminum-induced neuronal damage through attenuation of TNF-α, caspase-3, and DNA oxidation

Exposure is aluminum is on the increase with consequential neuronal damage. This study aimed to assess the neuroprotective effects of ribose-L-cysteine (Rlc) against aluminum-induced oxidative stress by evaluating various biochemical markers of, and histological changes in the hippocampus. The rats were divided into five groups: control, aluminum (Al3), Rlc alone, Al pre-treated with Rlc (Rlc/Al3), and Al post-treated with Rlc (Al/Rlc). Aluminum was administered for two weeks to induce neurotoxicity. Rlc was either given before or after Al's intoxication. Neurochemical markers (serotonin, dopamine, GSH, SOD, G6PD, catalase, MDA, TNF-alpha) were measured. Histological assessments using H&E and GFAP staining were performed to examine hippocampal architecture. The study investigated the effects of Ribose-L-Cysteine (Rlc) on various biochemical markers following aluminum-induced oxidative stress. Aluminum (Al3) administration significantly lowered serotonin, dopamine, G6PD, catalase, glutathione (GSH), and superoxide dismutase (SOD) and increased TNF-alpha and MDA levels. A two-week Rlc treatment post-Al3 exposure significantly elevated these protective enzymes and neurotransmitters in the Al3/Rlc group. However, pre-treatment with Rlc did not improve these markers in the Rlc/Al3 group, indicating the greater efficacy of post-exposure intervention. Rlc alone did not significantly alter these biomarkers compared to control, confirming its neuroprotective potential post-Al intoxication. Rlc significantly elevated serotonin, dopamine, GSH, catalase, and SOD levels post-Al exposure, reducing neurodegeneration, particularly in the Al/Rlc group.