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Melatonin reduces memory changes and neural oxidative damage in mice treated with D-galactose
Yu-Xian Shen1, Shu-Yun Xu, Wei Wei
1Institute of Clinical Pharmacology, Anhui Medical University, Hefei, China. shenyuxi@mail.hf.ah.cn
Journal of Pineal Research
|June 21, 2002
Summary
Melatonin administration improved learning and memory in D-galactose-induced amnesic mice. This neuroprotective effect is linked to melatonin
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- D-galactose induces cognitive deficits and oxidative stress in mice, mimicking aspects of brain aging.
- Reduced antioxidant enzyme activity and increased lipid peroxidation are observed in D-galactose-treated brains.
Purpose of the Study:
- To investigate the neuroprotective role of melatonin in a D-galactose-induced mouse model of amnesia.
- To evaluate the impact of melatonin on learning, memory, and oxidative stress markers.
Main Methods:
- Behavioral tests (avoidance/escape, water maze) assessed learning and memory.
- Spectrophotometry measured thiobarbituric acid-reactive substances (TBARS) and antioxidant enzyme activities (superoxide dismutase, glutathione peroxidase) in brain tissue.
Main Results:
- D-galactose significantly impaired learning and memory, increased TBARS, and decreased antioxidant enzyme activities.
- Melatonin treatment (0.1, 1, 10 mg/kg) dose-dependently reversed these D-galactose-induced changes.
- Melatonin administration blocked the decrease in learning and memory function and normalized oxidative stress markers.
Conclusions:
- D-galactose accelerates brain aging by promoting free radical generation and reducing antioxidant defenses.
- Melatonin exhibits significant antioxidative activity, improving cognitive function in this aging and amnesic model.
- Melatonin's neuroprotective effects are, at least partially, attributable to its ability to combat oxidative stress.