Association between dietary intake of α-tocopherol and cadmium related osteoporosis in population ≥ 50 years.

Introduction: To analyze the association between α-tocopherol intake and cadmium (Cd) exposure and osteoporosis in population ≥ 50 years.

Materials And Methods: Sociodemographic data, physical examination, and laboratory indicators including serum Cd level and dietary α-tocopherol intake of 8459 participants were extracted from the National Health and Nutrition Examination Survey (NHANES) database in this cross-sectional study. The associations between α-tocopherol intake, serum Cd levels and osteoporosis were evaluated using univariate and multivariate logistic regression analyses, with the estimated value (β), odds ratios (ORs) and 95% confidence intervals (CIs).

Co-exposure of cadmium and lead on bone health in a southwestern Chinese population aged 40-75 years.

Both cadmium (Cd) and lead (Pb) are associated with bone health, but studies exploring the effects of Cd and Pb co-exposure on bone health are rare. This study aimed to assess the interactive effects of Cd and Pb co-exposure on bone health. In total, 799 participants, living in the targeted areas (located in southwestern China) for more than 15 years, aged 40-75 years, and subsisted on homegrown rice and vegetables were investigated.

Benchmark dose estimation of urinary and blood cadmium as biomarkers of renal dysfunction among 40-75-year-old non-smoking women in rural areas of southwest China.

This study evaluated the association between urinary cadmium (U-Cd) and blood Cd (B-Cd) and several biomarkers of renal dysfunction (α -microglobulin [α -MG], β -microglobulin [β -MG], N-acetyl-β-d-glucosaminidase, metallothionein, retinol-binding protein and microalbumin [mALB]) and identified the biomarker(s) that was most closely correlated with U-Cd and B-Cd among female residents in rural areas of southwest China. U-Cd, creatinine (Cr), B-Cd and the above-mentioned six biomarkers in morning spot urine samples were measured from 288 randomly selected 40-75-year-old non-smoking women from non-polluted areas and Cd-polluted-areas. The lower 95% confidence limit of the benchmark dose (BMD) corresponding to the 5% (BMDL ) and 10% benchmark response (BMDL ) was calculated with assumed cut-off values of the 95th and 90th percentile.

Dietary cadmium exposure assessment in rural areas of Southwest China.

Dietary exposure of cadmium (Cd) has not been studied in Southwest China. The objective of the study was to determine the pollution characteristics and contamination levels in various agriculture products in Southwest China and to conduct a comparison of dietary exposure assessment of Cd in polluted and non-polluted areas. Results showed that the mean Cd contents in rice were 0.

Epigallocatechin-3-gallate confers protection against corticosterone-induced neuron injuries via restoring extracellular signal-regulated kinase 1/2 and phosphatidylinositol-3 kinase/protein kinase B signaling pathways.

Extensive studies suggested epigallocatechin-3-gallate (EGCG) has significant neuroprotection against multiple central neural injuries, but the underlying mechanisms still remain poorly elucidated. Here we provide evidence to support the possible involvement of extracellular signal-regulated kinase 1/2 (ERK1/2) and phosphatidylinositol-3 kinase/ protein kinase B (PI3K/AKT) pathways in EGCG-mediated protection against corticosterone-induced neuron injuries. As an essential stress hormone, corticosterone could induce obvious neurotoxicity in primary hippocampal neurons.

Involvement of PKCα and ERK1/2 signaling pathways in EGCG's protection against stress-induced neural injuries in Wistar rats.

Stress-induced neural injuries are closely linked to the pathogenesis of various neuropsychiatric disorders and psychosomatic diseases. We and others have previously demonstrated certain protective effects of epigallocatechin-3-gallate (EGCG) in stress-induced cerebral impairments, but the underlying protective mechanisms still remain poorly elucidated. Here we provide evidence to support the possible involvement of PKCα and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathways in EGCG-mediated protection against restraint stress-induced neural injuries in rats.