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D-Ribose-LCysteine attenuates manganese-induced cognitive and motor deficit, oxidative damage, and reactive microglia
Grace T Akingbade1, Omamuyovwi M Ijomone2, Aminu Imam3
1Department of Anatomy, Faculty of Basic Medical Sciences, University of Ilorin, Nigeria; The Neuro- Lab, Department of Human Anatomy, School of Basic Medical Sciences, Federal University of Technology Akure, Nigeria; Department of Molecular Pharmacology, Albert Einstein College of Medicine, NY, USA.
Abstract:
Due to overexposure, manganese (Mn) accumulation in the brain can trigger the inhibition of glutathione synthesis and lead to increased generation of reactive oxygen species (ROS) and oxidative stress. D-Ribose-L-Cysteine (RibCys) has been demonstrated to effectively support glutathione synthesis to scavenge ROS and protect cells from oxidative damage. In the present study, we examined the effects of RibCys on weight changes, cognitive and motor associated activities, oxidative stress markers, striatal and cortical histology, and microglia activation following Mn exposure. Rats were exposed to either saline, Mn or/and RibCys for two weeks. The Mn exposed rats received RibCys either as pre-, co-, or post-treatments. Mn caused a significant decrease in weight, memory and motor activities, increased lactate dehydrogenase level, overexpression of IBA1 reflecting microglia activation, and distortion of the neuronal cytoarchitecture of the striatum and motor cortex, respectively. Interventions with RibCys mitigated Mn-induced neurotoxic events. Our novel study demonstrates that RibCys effectively ameliorates the neurotoxicity following Mn treatment and maybe a therapeutic strategy against the neurological consequences of Mn overexposurec.
Insights
Manganese (Mn) brain exposure causes neurotoxicity. D-Ribose-L-Cysteine (RibCys) effectively reversed Mn-induced damage, protecting cognitive and motor functions by reducing oxidative stress.
Area of Science:
- Neuroscience
- Toxicology
- Biochemistry
Background:
- Manganese (Mn) overexposure leads to brain accumulation, inhibiting glutathione synthesis.
- This results in increased reactive oxygen species (ROS) and oxidative stress, causing neurotoxicity.
- D-Ribose-L-Cysteine (RibCys) supports glutathione synthesis and scavenges ROS.
Purpose of the Study:
- To investigate the neuroprotective effects of RibCys against manganese-induced toxicity.
- To assess RibCys's impact on weight, cognitive and motor functions, oxidative stress, and brain histology.
Main Methods:
- Rats were exposed to saline, Mn, or Mn plus RibCys (pre-, co-, or post-treatment) for two weeks.
- Evaluated weight changes, cognitive and motor activities, oxidative stress markers (lactate dehydrogenase), and microglia activation (IBA1).
- Histological analysis of striatal and cortical tissues was performed.
Main Results:
- Mn exposure significantly decreased weight, memory, and motor activities.
- Mn increased lactate dehydrogenase levels and IBA1 expression, indicating oxidative stress and microglia activation.
- Mn exposure distorted striatal and cortical neuronal cytoarchitecture.
- RibCys interventions mitigated Mn-induced neurotoxic effects across all treatment timings.
Conclusions:
- RibCys effectively ameliorates neurotoxicity caused by manganese overexposure.
- RibCys demonstrates potential as a therapeutic strategy for neurological damage from manganese.
- This study highlights RibCys's role in mitigating oxidative stress and neuroinflammation.
