ABSTRACT
BACKGROUND: In this report, the effects of long-term pulsed electromagnetic field (PEMF) exposure on hepatic and immunologic functions were examined. METHODS: Male rats were randomly divided into four groups: a control group and three experimental groups exposed to a 50-Hz PEMF at 5, 10, or 20 mT for 10 weeks. RESULTS: Compared with the control group, activities of serum alanine aminotransferase and aspartate aminotransferase and concentrations of serum, liver, and spleen Metabolism of lipid peroxidation (MDA) in the 10- and 20-mT PEMF groups were significantly increased. The activities of Glutathione peroxidase (GSH-Px) and Superoxide Dismutase (SOD) in the serum, liver, and spleen and concentrations of serum immunoglobulins were significantly decreased. CONCLUSION: These results demonstrate that long-term exposure to PEMF can lead to oxidative damage of the liver and spleen.
Subject(s)
Electromagnetic Fields , Immunity, Innate/immunology , Liver/immunology , Oxidative Stress/immunology , Spleen/immunology , Absorption, Radiation , Animals , Cytokines/immunology , Dose-Response Relationship, Radiation , Environmental Exposure , Immunity, Innate/radiation effects , Liver/radiation effects , Longitudinal Studies , Male , Oxidative Stress/radiation effects , Radiation Dosage , Rats , Rats, Wistar , Spleen/radiation effects , Whole-Body Irradiation/methodsABSTRACT
Melatonin is an endogenous antioxidant and free radical scavenger. A transgenic (Tg) mouse model for Alzheimer's disease mimics the accumulation of senile plaques, neuronal apoptosis and memory impairment. Previous studies indicated that melatonin reduced beta-amyloid (Abeta)-induced neurotoxicity. In this study, after giving melatonin at 10 mg/kg to APP 695 transgenic (APP 695 Tg) mice for 4 months, we evaluated the long-term influence of melatonin on behavior, biochemical and neuropathologic changes in APP 695 Tg mice. Step-down and step-through passive avoidance tests suggested that 8-month-old APP 695 Tg mice showed decreases in step-down latency and step-through latency and increases in count of error throughout the entire learning trial and memory session, which suggested learning and memory impairment. However, melatonin alleviated learning and memory deficits. Additionally, choline acetyltransferase (ChAT) activity also decreased in the frontal cortex and hippocampus of APP 695 Tg mice compared with non-Tg littermates. Melatonin supplementation increased ChAT activity in the frontal cortex and hippocampus. DNA fragmentation was present in the frontal cortex of the APP 695 Tg mice; melatonin reduced the number of apoptotic neurons. Congo Red staining and Bielschowsky silver impregnation both showed the apparent extracellular Abeta deposition in frontal cortex of APP 695 Tg mice. However, melatonin decreased the Abeta deposits. Our results indicate that neuroprotection by melatonin is partly related to modulation of apoptosis and protection of the cholinergic system. Early rational melatonin interventions may be one of the most promising strategies in the development of approaches to retard or prevent Abeta-mediated disease progression.
