Heavy metals play an important endocrine-disrupting role in the health consequences. However, the endocrine-disrupting mechanism of heavy metals is unclear. There are long-term and low-level metal/element exposure scenes for the human body in real life. Therefore, animal models exposed to high doses of heavy metals may not provide key information to elucidate the underlying pathogeny of human diseases. This review collects current knowledge regarding the endocrine-disrupting roles of heavy metals such as lead (Pb), cadmium (Cd), arsenic (As), mercury (Hg), nickel (Ni), copper (Cu), zinc (Zn), and manganese (Mn), summarizes the possible molecular mechanisms of these endocrine-disrupting chemicals (EDCs), and briefly evaluates their endocrine toxicity on animals and humans.

Recent studies have shown that some adverse pregnancy outcomes, especially intrauterine growth restriction (IUGR), are associated with gestational exposure to ambient fine particulate matter (PM_2.5). However, potential mechanism remains to be elucidated. In the present study, pregnant C57BL/6 mice were randomly assigned to be exposed to either filtered air or ambient PM_2.5 in the gestation period via a concentrated whole-body exposure system. We found that gestational PM_2.5 exposure exerted no effect on implantation, preterm delivery, as well as fetal resorption and death. However, in utero fetal exposure to PM_2.5 showed a significant reduction in body weight and crown-rump length on GD13 and GD18. Meanwhile, maternal blood sinusoid in placenta was markedly reduced along with abnormal expression of placental nutrient transporters and growth hormone in dams exposed to PM_2.5. Additional tests showed gestational PM_2.5 exposure decreased autophagy-related protein levels and inhibited autophagy flux mainly on GD15. Correspondingly, AMPK/mTOR signaling pathway, a critical negative regulator of autophagy, was activated in placenta on GD15 by PM_2.5 exposure as well. These findings provide evidences that placental developmental disorder caused by autophagy inhibition might be an important mechanism for the growth restriction caused by PM_2.5 exposure.

Emerging evidence suggests that exposure to airborne fine particulate matter (PM_2.5) is closely related to disturbances in hepatic lipid metabolism. However, no systematic study assessed the age vulnerability in effects of PM_2.5 exposure on metabolism, and the potential mechanisms remain unknown. This study aimed to investigate the metabolic susceptibility of different life stages to PM_2.5 exposure, and to evaluate the underlying molecular mechanisms. Male C57BL/6 mice at three life phases (young, adult, and middle-aged) were exposed simultaneously to concentrated ambient PM_2.5 or filtered air (FA) for 8 weeks using a whole-body inhalational exposure system. The average daily PM_2.5 concentrations to which mice were actually exposed were 90.71 ± 7.99 μg/m³. The body weight, total food utilization, body composition, glucose metabolic homeostasis of the mice were evaluated. At euthanasia, serum and liver samples were collected to measure lipid profiles and hepatic function. H&E and Oil Red O staining were used to assess the liver cellular structure and hepatic lipid deposition. Transcriptomics and lipidomics were performed to determine the differentially expressed genes and lipid metabolites in the liver. Quantitative RT-PCR and immunoblots were performed to verify the transcriptomics and explore the mechanism for metabolic susceptibility. PM_2.5 exposure led to reductions in body weight gain, total food utilization, and fat mass in middle-aged mice but not in young or adults. Exposure to PM_2.5 reduced hepatic lipid deposition by enhancing lipolysis and inhibiting the glycerol-3-phosphate (G3P) pathway of hepatic lipogenesis. Furthermore, PM_2.5 exposure attenuated hepatic fatty acid metabolism and primary bile acid biosynthesis. Finally, PM_2.5 exposure dysregulated hepatic phospholipid metabolism, as evidenced by increased glycerophospholipid synthesis and disturbed sphingolipid metabolism. Therefore, middle-aged male mice were more vulnerable to PM_2.5 exposure with double-edged effects, improved metabolism and hepatic TG accumulation but inhibited hepatic fatty acid and bile acid metabolism and dysregulated phospholipid metabolism.

It is well known that extreme heat events happen frequently due to climate change. However, studies examining the direct health impacts of increased temperature and heat waves are lacking. Previous reports revealed that heatstroke induced acute lung injury and pulmonary dysfunction. This study aimed to investigate whether heat exposure induced lung fibrosis and to explore the underlying mechanisms. Male C57BL/6 mice were exposed to an ambient temperature of 39.5 ± 0.5 °C until their core temperature reached the maximum or heat exhaustion state. Lung fibrosis was observed in the lungs of heat-exposed mice, with extensive collagen deposition and the elevated expression of fibrosis molecules, including transforming growth factor-β1 (TGF-β1) and Fibronectin (Fn1) (p < 0.05). Moreover, epithelial–mesenchymal transition (EMT) occurred in response to heat exposure, evidenced by E-cadherin, an epithelial marker, which was downregulated, whereas markers of EMT, such as connective tissue growth factor (CTGF) and the zinc finger transcriptional repressor protein Slug, were upregulated in the heat-exposed lung tissues of mice (p < 0.05). Subsequently, cell senescence examination revealed that the levels of both senescence-associated β-galactosidase (SA-β-gal) staining and the cell cycle protein kinase inhibitor p21 were significantly elevated (p < 0.05). Mechanistically, the cGAS–STING signaling pathway evoked by DNA damage was activated in response to heat exposure (p < 0.05). In summary, we reported a new finding that heat exposure contributed to the development of early pulmonary fibrosis-like changes through the DNA damage-activated cGAS–STING pathway followed by cellular senescence.

Background: Understanding undergraduates’ dietary literacy, including dietary knowledge, attitude and practice (KAP), is important for future health promotion policies. Therefore, this study aimed to investigate the current status and influencing factors of dietary literacy in Chinese college undergraduates and explore whether a nutritional lecture could improve their dietary literacy. Methods: This study included two parts: a cross-sectional study (n = 1026) conducted by a dietary literacy questionnaire, and a randomized controlled trail (RCT) that enrolled 99 college undergraduates who were randomized to a control group or a nutritional lecture group. Data from the questionnaire and 72 h food records were obtained on day 0, day 3 and day 100 before and after intervention. Results: This cross-sectional study showed that the mean scores of dietary KAP were respectively 100.0 (33.3), 59.1 (13.6) and 71.7 (11.7), with an excellent rate of 36.6%, 1.9% and 3.4%. Female upper-grade undergraduates and those with medicine-related majors illustrated higher dietary knowledge scores (p < 0.001). Dietary attitude rather than dietary knowledge had a significant impact on dietary practice (p < 0.001). This finding was in line with the results in the RCT study. Compared with the control group, dietary knowledge was significantly improved in the nutritional lecture group on both day 3 (p = 0.002) and day 100 (p = 0.023) after intervention. However, dietary behavior was improved only on day 3 post nutritional lecture (p = 0.029) but decreased to the original level 100 days later (p < 0.001). Conclusions: This study discovered the unsatisfying status and discrepancy between dietary literacy among college undergraduates of different sex, majors and college years. Dietary attitude instead of dietary knowledge was discovered as a determining role in dietary practice. One nutritional lecture could improve undergraduates’ dietary literacy but the effect was not long-lasting. Further studies with more reinforced and durable interventions are warranted.

Both epidemiological and experimental studies increasingly show that exposure to ambient fine particulate matter (PM2.5) is related to the occurrence and development of chronic diseases, such as metabolic diseases. However, whether PM2.5 has "exposure memory" and how these memories affect chronic disease development like hepatic metabolic homeostasis are unknown. Therefore, we aimed to explore the effects of exposure transition on liver cholesterol and bile acids (BAs) metabolism in mice. In this study, C57BL/6 mice were exposed to concentrated ambient PM2.5 or filtered air (FA) in a whole-body exposure facility for an initial period of 10 weeks, followed by another 8 weeks of exposure switch (PM2.5 to FA and FA to PM2.5) comparing to non-switch groups (FA to FA and PM2.5 to PM2.5), which were finally divided into four groups (FF of FA to FA, PP of PM2.5 to PM2.5, PF of PM2.5 to FA, and FP of FA to PM2.5). Our results showed no significant difference in food intake, body composition, glucose homeostasis, and lipid metabolism between FA and PM2.5 groups after the initial exposure before the exposure switch. At the end of the exposure switch, the mice switched from FA to PM2.5 exposure exhibited a high sensitivity to late-onset PM2.5 exposure, as indicated by significantly elevated hepatic cholesterol levels and disturbed BAs metabolism. However, the mice switched from PM2.5 to FA exposure retained a certain memorial effects of previous PM2.5 exposure in hepatic cholesterol levels, cholesterol metabolism, and BAs metabolism. Furthermore, 18-week PM2.5 exposure significantly increased hepatic free BAs levels, which were completely reversed by the FA exposure switch. Finally, the changes in small heterodimeric partner (SHP) and nuclear receptor subfamily 5 group A member 2 (LRH1) in response to exposure switch mechanistically explained the above alterations. Therefore, mice switching from PM2.5 exposure to FA showed only a weak memory of prior PM2.5 exposure. In contrast, the early FA caused mice to be more susceptible to subsequent PM2.5 exposure.