Parkinson’s disease (PD) is a gradually progressing neurodegenerative condition that is marked by a loss of motor coordination along with non-motor features. Although the precise cause of PD has not been determined, the disease condition is mostly associated with the exposure to environmental toxins, such as metals, and their abnormal accumulation in the brain. Heavy metals, such as iron (Fe), mercury (Hg), manganese (Mn), copper (Cu), and lead (Pb), have been linked to PD and contribute to its progression. In addition, the interactions among the components of a metal mixture may result in synergistic toxicity. Numerous epidemiological studies have demonstrated a connection between PD and either single or mixed exposure to these heavy metals, which increase the prevalence of PD. Chronic exposure to heavy metals is related to the activation of proinflammatory cytokines resulting in neuronal loss through neuroinflammation. Similarly, metals disrupt redox homeostasis while inducing free radical production and decreasing antioxidant levels in the substantia nigra. Furthermore, these metals alter molecular processes and result in oxidative stress, DNA damage, mitochondrial dysfunction, and apoptosis, which can potentially trigger dopaminergic neurodegenerative disorders. This review focuses on the roles of Hg, Pb, Mn, Cu, and Fe in the development and progression of PD. Moreover, it explores the plausible roles of heavy metals in neurodegenerative mechanisms that facilitate the development of PD. A better understanding of the mechanisms underlying metal toxicities will enable the establishment of novel therapeutic approaches to prevent or cure PD.

Humans are exposed to lead (Pb), mercury (Hg), and cadmium (Cd) through various routes, including drinking water, and such exposure can lead to a range of toxicological effects. However, few studies have investigated the toxic effects of exposure to mixtures of metals, particularly in relation to neurotoxicity. In this study, 7-week-old male mice were exposed to Pb, Hg, and Cd individually or in combination through their drinking water for 28 days. The mice exposed to the metal mixture exhibited significantly reduced motor coordination and impaired learning and memory abilities compared to the control group and each of the single metal exposure groups, indicating a higher level of neurotoxicity of the metal mixture. The dopamine content in the striatum was significantly lower in the metal mixture exposure group than in the single metal exposure groups and the control group. Furthermore, compared to the control group, the metal mixture exposure group showed a significantly lower expression level of tyrosine hydroxylase (TH) and significantly higher expression levels of dopamine transporter (DAT), tryptophan hydroxylase 1 (TPH1), and serotonin reuptake transporter (SERT). Notably, there were no significant differences in SERT expression between the single metal exposure groups and the control group, but SERT expression was significantly higher in the metal mixture exposure group than in the single metal and control groups. These findings suggest that the key proteins involved in the synthesis and reuptake of dopamine (TH and DAT, respectively), as well as in the synthesis and reuptake of serotonin (TPH1 and SERT, respectively), play crucial roles in the neurotoxic effects associated with exposure to metal mixtures. In conclusion, this study demonstrates that simultaneous exposure to different metals can impact key enzymes involved in dopaminergic and serotonergic neurotransmission processes, leading to disruptions in dopamine and serotonin homeostasis and consequently a range of detrimental neurobehavioral effects.

Aims: Alcohol consumption is known to be closely related with alterations in blood lipid levels as well as in blood pressure. The objective of this study was to evaluate the association between alcohol consumption and blood lipid levels in hypertensive men. Methods: A cross-sectional study involving participants (n = 2014) aged 20–69 years from the Korea National Health and Nutrition Examination Survey, 1998–2009. Demographic characteristics, dietary intake and medical history were obtained from the participants by questionnaire, and lipid levels were determined by analysis of blood samples. Results: After adjusting for demographic and dietary factors, alcohol consumption was negatively associated with risk of low high-density lipoprotein cholesterol [HDL-C; odds ratio (OR): 0.29, 95% confidence interval (CI): 0.22–0.40 in heavy (≥30 g/day) drinkers; P for trend <0.001], whereas the risk of high triglycerides increased with increasing alcohol consumption (OR: 2.04, 95% CI: 1.53–2.72 in heavy drinkers; P for trend <0.001). However, the OR of high non-HDL-C and the ratio of high triglycerides to HDL-C did not change significantly with an increase in alcohol consumption. Conclusion: These data suggest that alcohol consumption differentially affected lipid measures according to the amount of alcohol intake in hypertensive men.

The effect of commonly used oral contraceptives (OCs) on blood pressure is still unclear. The aim of this study was to examine the relationship between OCs use and blood pressure and the prevalence of hypertension in a population-based sample of Korean women.