Selenium (Se) is an essential trace element known for its significant role in maintaining human health and mitigating disease progression. Selenium and its compounds exhibit high selective cytotoxicity against tumor cells. However, their anti-cervical cancer (CC) effects and underlying mechanisms have not been fully explored. This study found that sodium selenite (SS) inhibits the viability of HeLa and SiHa cells in a dose- and time-dependent manner. Intraperitoneal injection of 3 and 6 mg/kg SS for 14 days in female nude mice significantly inhibited the growth of HeLa cell xenografts without evident hepatotoxicity or nephrotoxicity. RNA sequencing results indicated that the AMP-activated protein kinase (AMPK), Forkhead box protein O (FOXO), and apoptosis signaling pathways are key regulatory pathways in SS’s anti-CC effects, and SS’s inhibition of HeLa cell proliferation may be related to autophagy and ROS-induced apoptosis. Further research has revealed that SS induces cell autophagy and apoptosis through the AMPK/mTOR/FOXO3a pathway, characterized by the upregulation of p-AMPK/AMPK, FOXO3a, LC3-II, cleaved-caspase3, and cleaved-PARP and the downregulation of p-mTOR/mTOR and p62. Additionally, SS impaired mitochondrial function, including decreased mitochondrial membrane potential, mitochondrial Ca²⁺ overload, and accumulation of mitochondrial reactive oxygen species (mtROS). Pretreatment with Mitoquinone mesylate (Mito Q) and compound C partially reversed SS-induced apoptosis, autophagy, and proliferation inhibition. Pretreatment with 3-methyladenine (3-MA) enhances SS-induced apoptosis and proliferation inhibition in HeLa cells but reverses these effects in SiHa cells. In summary, SS induces apoptosis, autophagy, and proliferation inhibition in HeLa and SiHa cells through the activation of the AMPK/mTOR/FOXO3a signaling pathway via mtROS. Autophagy activation may be a major risk factor for SS-induced apoptosis in SiHa cells but can protect HeLa cells from SS-induced apoptosis. These findings provide new evidence for understanding the molecular mechanisms underlying SS in potential new drug development for CC.

Few researchers have studied the national prevalence of Keshan disease (KD) in China using spatial epidemiological methods. This study aimed to provide geographically precise and visualized evidence for the strategies for KD prevention and control. We surveyed and analyzed 237,000 people in 280 out of 328 KD-endemic counties (85.4%) in mainland China using a design of key investigation based on case-searching in 2015–2016. ArcGIS version 9.0 was used for spatial autocorrelation analysis, spatial interpolation analysis and spatial regression analysis. Global autocorrelation analysis showed that global clustering of latent Keshan disease (LKD) prevalence was noted (Moran’s I = 0.22, Z = 7.06, and P < 0.0001), no global clustering of chronic Keshan disease (CKD) prevalence (Moran’s I = 0.03, Z = 1.10, and P = 0.27) was observed. Spatial regression analysis showed that LKD prevalence was negatively correlated with per capita disposable income (t = –4.36, P < 0.0001). Local autocorrelation analysis at the county level effectively identified the cluster areas of LKD prevalence in the provinces of Shaanxi, Gansu, Shanxi, Inner Mongolia, and Jilin. The high-high cluster areas should be given priority for precision prevention and control of Keshan disease. This spatial epidemiological study revealed that LKD prevention and control should be strengthened in areas with high values of clustering. Our findings provided spatially, geographically precise and visualized evidence for prioritizing KD prevention and control.

Background: Selenium (Se) is an essential trace element for maintaining human health, with significant antioxidant and immunoregulatory functions. Inadequate Se intake may be associated with Keshan disease, Kashin–Beck disease, and hypothyroidism. However, effective indicators for scientifically guiding Se supplementation in Se-deficient populations are still lacking. Objectives: This study aims to explore the dynamic distribution of Se across various nutritional biomarkers and major organs in rats through a Se supplementation experiment, as well as the pairwise correlations between them, in order to identify reliable nutritional indicators for evaluating Se levels in the body. Methods: Se levels in hair, blood, and major tissues and organs were determined by atomic fluorescence spectrometry, and glutathione peroxidase (GSH-Px) levels were measured using an ELISA. Results: Se supplementation significantly increased Se levels in rat blood, hair, and major organs, as well as GSH-Px levels in blood. Se primarily accumulated in the liver and kidneys, followed by myocardium, spleen, and muscles. Serum and plasma Se were found to be the best indicators of short-term Se intake, while erythrocyte Se levels showed a stronger correlation with Se levels in tissues and organs, making it a better marker for assessing long-term Se nutritional status compared to hair Se. Conclusions: This study demonstrates the potential of erythrocyte Se levels as an indicator for evaluating long-term Se nutritional status, providing scientific evidence for Se nutritional assessments.

Background: Cancer surveillance in Mainland China is based on household-registered residents (HRR) and therefore fails to cover migrant populations. This introduces selection bias and leads to a misestimation of the true cancer burden. Estimating lung cancer (LC) incidence and mortality among resident populations (RPs) provides a more accurate epidemiological and public health assessment. Methods: Using 2016 data from 487 cancer registries and multidimensional covariates, we developed a Bayesian-integrated nested Laplace approximation with stochastic partial differential equation (INLA-SPDE) model to estimate LC incidence and mortality among the RP, with adjustments for interprovincial migration. Results: In 2016, the interprovincial migrant population in Mainland China reached 140.96 million, representing 10.1% of the HRR. The results indicate that the INLA-SPDE model outperformed the Bayesian hierarchical linear model in estimation accuracy, effectively captured spatial heterogeneity and achieved a Bayesian credible interval coverage exceeding 94%. Significant disparities in LC incident cases and deaths between RPs and HRR were observed in Henan (9159 cases and 7539 deaths), Guangdong (8851 cases and 7235 deaths), and Shanghai (5406 cases and 4332 deaths). The largest rate differences occurred in Shanghai (incidence, 20.4/100 000, 23.7%; mortality, 8.7/100 000, 15.1%). Conclusion: Disparities in incidence and mortality vary with the direction and magnitude of interprovincial migration, indicating that household-registered residency-based registration overestimates LC burden in high-immigration regions and underestimates it in high-emigration regions. We recommend transitioning to RP-based registration to improve the accuracy of LC burden estimates of cancer surveillance, particularly in regions with substantial migrant populations.

Selenium deficiency is an established etiological risk factor for Keshan disease, yet conventional biomarkers and linear modeling approaches remain insufficient for capturing its complex metabolic dynamics. This study aims to elucidate the nonlinear dynamics of selenium biomarkers for precision prevention of Keshan disease. This study employed a human-rat dual-system design and a multi-model analytical framework. The human cohort included 6987 adults from 29 Chinese provinces, stratified by endemicity. The animal experiment utilized 100 specific-pathogen-free male Wistar rats, randomly allocated into a control group and a sodium selenite intervention group (200 μg/L), with samples collected across five sequential stages. Biospecimens including blood, hair, and myocardial tissue were systematically analyzed for selenium content, selenoprotein P, and glutathione peroxidase activity. In statistical analyses, we employed a multi-model comparison strategy incorporating generalized additive models, polynomial regression, restricted cubic splines, and linear regression to identify the optimal approach for analyzing selenium biomarker dynamics. In human populations, serum selenium in non-endemic areas showed an initial increase followed by a decline with rising hair selenium, while endemic areas exhibited a sustained but gradually saturating increase. Rat experiments revealed strengthening correlations between myocardial selenium and both erythrocyte and hair selenium (r_s > 0.6) after prolonged supplementation, with nonlinear models uncovering saturation kinetics. Myocardial selenium rose rapidly and then plateaued relative to serum glutathione peroxidase activity, but remained inversely correlated with serum selenoprotein P. Generalized additive models outperformed other approaches in describing myocardial-peripheral biomarker associations. Selenium biomarkers exhibit dynamic, non-linear associations. Erythrocyte selenium reflects myocardial status, whereas serum selenoprotein P and glutathione peroxidase activity respectively serve as long-term and short-term indicators. Keshan disease involves threshold-saturation-driven systemic selenium dysregulation, not mere deficiency. Non-linear myocardial selenium accumulation favors continuous, moderate over short-term, high-dose supplementation, supporting precision assessment and prevention in endemic areas.