ABSTRACT
PURPOSE: Many age-related structural and functional changes in the brain have important consequences. Long-term exposure to mercury and the impact of functional polymorphisms of metal-regulating proteins such as metallothioneins (MTs) can result in neurological-neurobehavioral effects in elderly individuals. Therefore, the aims of this study are to examine the associations between biomarkers of mercury exposure and cognitive impairment and to investigate the effect of the rs8052394 single nucleotide polymorphism (SNP) of the potential modifier gene MT1A on different domains of the Montreal Cognitive Assessment (MoCA). MATERIALS AND METHODS: We studied 436 participants aged ≥55 years from the Electricity Generating Authority of Thailand study. They underwent a physical examination, an extensive cognitive assessment with the MoCA (cutoff <26 points), and a biochemical analysis related to diabetes and dyslipidemia. The blood mercury level was determined by inductively coupled plasma mass spectrometry. Genotyping of the MT1A rs8052394 SNP was performed by the restriction fragmentation length polymorphism method. RESULTS: The mean age of the study population was 58.8±3.01 years, and most had ≥12 years of education (75.7%). The primary study finding was that the prevalence of mild cognitive impairment (MCI) in older Thai adults was 39.7%. The frequency distributions of the G allele of the rs8052394 SNP of the MT1A gene were significantly associated with the total and sub-domain MoCA scores. The prevalence of MCI was significantly associated with increased age, hypertriglyceridemia, hyperhomocysteinemia, the third tertile of blood mercury concentration, and the rs8052394 variant genotype of MT1A (P values for all odds ratios <0.05). CONCLUSION: These findings suggested that neurocognitive effects associate with mercury exposure and genetic susceptibility in toxicokinetics. Public health strategies can be used to implement as a comprehensive action plan to educate vulnerable populations on how to reduce mercury exposure. Concurrently, impact of such genetic predisposition requires replication for identifying and protecting susceptible individuals from mercury toxicity.
ABSTRACT
BACKGROUND: Effects of the micronutrient selenium have been proposed in obesity and type 2 diabetes mellitus (T2DM) that involve impairments in glucose metabolic pathways and the insulin signaling cascade, mediated through oxidative stress and inflammation. However, the evidence collected to date through animal and epidemiologic studies has been inconclusive. Therefore, in the present study, we aimed to evaluate the relationships of selenium status and inflammation with T2DM and obesity. METHODS: Participants in the re-survey of the Electricity Generating Authority of Thailand (EGAT)2 study conducted in 2013 (N=655, age 45-60 years) were allocated to three groups based on their body mass index (World Health Organization Asia-Pacific Classification), and their serum selenium and high-sensitivity C-reactive protein (hs-CRP) concentrations and other clinical parameters were compared. RESULTS: Significant differences in serum selenium and hs-CRP among the groups were associated with differences in fasting blood glucose and glycated hemoglobin, as well as differences in the prevalence of prediabetes or T2DM. The adjusted odds ratios (ORs) (95% confidence intervals) for prediabetes or diabetes were 1.991 (1.318-3.009) and 3.786 (2.087-6.896) for the lowest and highest tertiles of serum selenium concentration in the entire sample and obese participants, respectively. Furthermore, the rising extent of hs-CRP increased the significantly associated with prediabetes or diabetes (adjusted ORs; 2.268 for the entire sample, 4.043 for the overweight and 1.910 for the obesity). CONCLUSION: Selenium status may be linked to both obesity and T2DM through its effects on signaling pathways. Further nutrigenomic studies are required to clarify the relationship between selenium and metabolic diseases.
ABSTRACT
Lead has been linked to the development of hypertension via oxidative stress. Catalase plays an important role in the disposal of hydrogen peroxide in erythrocyte and its activity was determined by CAT gene. The aims of this study were to investigate (1) the association between blood levels of antioxidant markers such as catalase, superoxide dismutase, glutathione, glutathione peroxidase, oxidative stress-marker (malondialdehyde), and blood lead level and (2) the influence of genetic polymorphism of CAT gene (rs769217) on change in blood pressure in general population of EGAT study project. This is a cross-sectional study of 332 normotensive, 432 prehypertensive, and 222 hypertensive male subjects. Hypertensive subjects had significantly higher blood lead level (5.28 µg/dL) compared to normotensive (4.41 µg/dL) and prehypertensive (4.55 µg/dL) subjects (P < 0.05). These significant findings are also found in MDA levels. Moreover, individuals with TT genotype in hypertensive group had significantly higher blood lead and MDA levels (6.06 µg/dL and 9.67 µmol/L) than those with CC genotype (5.32 µg/dL and 8.31 µmol/L, P < 0.05). Our findings suggested that decreased blood catalase activity in this polymorphism together with low level lead exposure induced lipid peroxidation may be responsible for hypertension.
