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Cardiovascular toxicities upon manganese exposure
1Department of Occupational Health and Toxicology, Guangxi Medical University, Nanning, Guangxi, PRC.
Abstract:
Manganese (Mn)-induced Parkinsonism has been well documented; however, little attention has been devoted to Mn-induced cardiovascular dysfunction. This review summarizes literature data from both animal and human studies on Mn's effect on cardiovascular function. Clinical and epidemiological evidence suggests that the incidence of abnormal electrocardiogram (ECG) is significantly higher in Mn-exposed workers than that in the control subjects. The main types of abnormal ECG include sinus tachycardia, sinus bradycardia, sinus arrhythmia, sinister megacardia, and ST-T changes. The accelerated heart-beat and shortened P-R interval appear to be more prominent in female exposed workers than in their male counterparts. Mn-exposed workers display a mean diastolic blood pressure that is significantly lower than that of the control subjects, especially in the young and female exposed workers. Animal studies indicate that Mn is capable of quickly accumulating in heart tissue, resulting in acute or subacute cardiovascular disorders, such as acute cardiodepression and hypotension. These toxic outcomes appear to be associated with Mn-induced mitochondrial damage and interaction with the calcium channel in the cardiovascular system.
Insights
Manganese exposure is linked to abnormal heart rhythms and lower blood pressure in workers. Animal studies show manganese accumulates in heart tissue, causing cardiovascular issues via mitochondrial damage.
Area of Science:
- Environmental Health
- Cardiology
- Toxicology
Background:
- Manganese (Mn) is known to cause Parkinsonism, but its cardiovascular effects are less understood.
- Existing literature provides limited data on manganese's impact on cardiovascular function.
Purpose of the Study:
- To review and summarize existing animal and human studies on manganese's effects on cardiovascular function.
- To highlight the association between manganese exposure and cardiovascular dysfunction.
Main Methods:
- Literature review of clinical, epidemiological, and animal studies.
- Analysis of electrocardiogram (ECG) abnormalities and blood pressure in manganese-exposed populations.
- Examination of animal models to understand manganese accumulation and cellular mechanisms in the heart.
Main Results:
- Manganese-exposed workers show a higher incidence of abnormal ECGs (e.g., tachycardia, bradycardia, ST-T changes).
- Accelerated heart rate and shortened P-R intervals are more pronounced in female exposed workers.
- Exposed workers, particularly young females, exhibit significantly lower diastolic blood pressure.
- Animal studies confirm rapid manganese accumulation in heart tissue, leading to cardiodepression and hypotension.
Conclusions:
- Manganese exposure poses a significant risk for cardiovascular dysfunction, including ECG abnormalities and hypotension.
- Manganese-induced cardiovascular toxicity is potentially mediated by mitochondrial damage and calcium channel interactions.
- Further research is warranted to fully elucidate the mechanisms and long-term cardiovascular consequences of manganese exposure.
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