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Decreased expression of inflammation-related genes following inhalation exposure to manganese
Diem HaMai1, Amber L Rinderknecht, Kaizhi Guo-Sharman
1Department of Community & Environmental Medicine, University of California, Irvine, CA 92697-1825, USA. diemh@uci.edu
Abstract:
Excessive exposure to manganese (Mn) by inhalation can induce psychosis and Parkinsonism. The clinical manifestations of Mn neurotoxicity have been related to numerous physiological and cellular processes, most notably dopamine depletion. However, few studies have explored the molecular events that are triggered in response to exposure to Mn by inhalation. In this current study, the transcriptional patterns of genes related to oxidative stress or inflammation were examined in the brain rats of exposed to inhaled Mn during either gestation or early adulthood. The expression of genes encoding for proteins critical to an inflammatory response and/or possessing pro-oxidant properties, including TGFbeta and nNOS, were slightly depressed by prenatal exposure, whereas inhalation exposure to Mn during adulthood markedly down-regulated their transcription. However, when exposures to manganese occurred during gestation, the extent of altered gene expression induced by subsequent exposure to Mn in adulthood was reduced. This suggests that prior exposure to Mn may have attenuated the effects of inhalation exposure to Mn in adulthood, in which the expression of inflammation-related genes were suppressed.
Insights
Inhaled manganese (Mn) exposure can cause neurotoxicity. Prenatal Mn exposure in rats reduced the impact of adult Mn exposure on inflammation-related gene expression, suggesting a protective effect.
Area of Science:
- Neuroscience
- Toxicology
- Molecular Biology
Background:
- Manganese (Mn) inhalation is linked to neurotoxicity, including psychosis and Parkinsonism.
- Dopamine depletion is a known consequence of Mn neurotoxicity.
- Molecular mechanisms underlying Mn inhalation neurotoxicity remain underexplored.
Purpose of the Study:
- To investigate the effects of inhaled manganese exposure on gene expression patterns.
- To examine transcriptional changes related to oxidative stress and inflammation in rat brains.
- To compare the impact of Mn exposure during gestation versus early adulthood.
Main Methods:
- Rats were exposed to inhaled manganese (Mn) during gestation or early adulthood.
- Transcriptional patterns of genes involved in inflammation and oxidative stress were analyzed.
- Specific genes examined included those encoding for TGFbeta and neuronal nitric oxide synthase (nNOS).
Main Results:
- Prenatal Mn exposure slightly decreased the expression of inflammation and pro-oxidant genes.
- Adult Mn exposure markedly down-regulated the transcription of these genes.
- Prior gestational Mn exposure attenuated the gene expression changes induced by subsequent adult Mn exposure.
Conclusions:
- Inhaled manganese exposure significantly alters gene expression related to inflammation and oxidative stress.
- Gestational manganese exposure may confer some protection against the neurotoxic effects of adult manganese inhalation.
- Further research is needed to elucidate the long-term molecular consequences of manganese exposure at different life stages.
