Association between nocturnal light exposure and melatonin in humans: a meta-analysis.

BACKGROUND: Night shift workers are more susceptible to circadian rhythm disturbances due to their prolonged exposure to nighttime light. This exposure during abnormal periods causes inappropriate suppression of melatonin synthesis and secretion in the pineal gland, thereby disrupting circadian rhythms. While it is believed that nocturnal light exposure is involved in suppressing melatonin secretion, research findings in this area have been inconsistent. METHODS: Thirteen publications retrieved from PubMed and Web of Science databases were included to compare the differences between night shift workers and controls using aggregated mean differences (MD) and 95% confidence intervals (CI). RESULTS: After a comprehensive review, 13 publications were included and data on urinary melatonin metabolite 6-sulfameoxymelatonin(aMT6s) were collected for meta-analysis. The results showed that the morning urinary aMT6s levels were significantly lower in the exposed group than in the non-exposed group (MD = -3.69, 95%CI = (-5.41, -1.98), P < 0.0001), with no significant heterogeneity among the original studies (I2 = 42%, P = 0.13). In addition, night shift workers had significantly lower mean levels of 24-h urinary aMT6s than day shift workers (MD = -3.38, 95%CI = (-4.27, -2.49), P < 0.00001, I2 = 0). Nocturnal light was correlated with nocturnal urine aMT6s secretion and inhibited nocturnal aMT6s secretion (MD = -11.68, 95%CI = (-15.70, -7.67), P < 0.00001, I2 = 0). Additionally, nocturnal light inhibited the secretion of melatonin in the blood, with no significant heterogeneity between studies (MD = -11.37, 95%CI = (-15.41, -7.33), P < 0.00001, I2 = 0). CONCLUSION: The findings of this study indicate that exposure to nocturnal light among night shift workers leads to inhibition of melatonin secretion.

Assessment of five typical environmental endocrine disruptors and thyroid cancer risk: a meta-analysis.

Introduction: There are conflicting reports on the association between environmental endocrine disruptors (EEDs) and thyroid cancer. This meta-analysis aimed to elucidate the relationship between EEDs and thyroid cancer. Methods: We searched for epidemiological studies on EEDs and thyroid cancer published in PubMed and Web of Science up to December 2022. We then screened the articles that could extract data on EEDs concentration levels in both thyroid cancer patients and healthy controls. We excluded articles that could not calculate effect sizes, focused on other thyroid diseases, or lacked controls. Standardized mean difference (SMD) was calculated to analyze the association between EEDs and thyroid cancer. We measured the heterogeneity among the included studies using I2, assessed publication bias by Egger's and Begg's test, and evaluated article quality using the Newcastle-Ottawa Quality Score (NOS). In the end, fifteen eligible case-control studies were included. Results: Our comprehensive analysis revealed that polychlorinated biphenyls (PCBs) were negatively associated with thyroid cancer{ SMD = -0.03, 95% confidence interval (CI) = (-0.05, -0.00), P = 0.03}, while polybrominated diphenyl ethers (PBDEs), phthalates (PAEs), and heavy metals were positively associated with thyroid cancer{PBDEs: SMD = 0.14, 95%CI = (0.04, 0.23), P = 0.007; PAEs: SMD = 0.30, 95%CI = (0.02, 0.58), P = 0.04; heavy metals: SMD = 0.21, 95%CI = (0.11, 0.32), P < 0.001}. We did not find a statistically significant relationship between bisphenol A (BPA) and thyroid cancer. Most of the included studies did not show publication bias, except for those on PCBs. Discussion: Our results indicate that exposure to certain EEDs, such as PBDEs, PAEs, and heavy metals, increases the risk of thyroid cancer. However, further large-scale epidemiological studies and mechanism studies are needed to verify these potential relationships and understand the underlying biological mechanisms.

Differential functions of RhoGDIß in malignant transformation and progression of urothelial cell following N-butyl-N-(4-hydmoxybutyl) nitrosamine exposure.

BACKGROUND: Functional role of Rho GDP-dissociation inhibitor beta (RhoGDIß) in tumor biology appears to be contradictory across various studies. Thus, the exploration of the molecular mechanisms underlying the differential functions of this protein in urinary bladder carcinogenesis is highly significant in the field. Here, RhoGDIß expression patterns, biological functions, and mechanisms leading to transformation and progression of human urothelial cells (UROtsa cells) were evaluated following varying lengths of exposure to the bladder carcinogen N-butyl-N-(4-hydmoxybutyl) nitrosamine (BBN). RESULTS: It was seen that compared to expression in vehicle-treated control cells, RhoGDIß protein expression was downregulated after 2-month of BBN exposure, but upregulated after 6-month of exposure. Assessments of cell function showed that RhoGDIß inhibited UROtsa cell growth in cells with BBN for 2-month exposure, whereas it promoted the invasion of cells treated with BBN for 6 months. Mechanistic studies revealed that 2-month of BBN exposure markedly attenuated DNMT3a abundance, and this led to reduced miR-219a promoter methylation, increased miR-219a binding to the RhoGDIß mRNA 3'UTR, and reduced RhoGDIß protein translation. While after 6-mo of BBN treatment, the cells showed increased PP2A/JNK/C-Jun axis phosphorylation and this in turn mediated overall RhoGDIß mRNA transcription and protein expression as well as invasion. CONCLUSIONS: These findings indicate that RhoGDIß is likely to inhibit the transformation of human urothelial cells during the early phase of BBN exposure, whereas it promotes invasion of the transformed/progressed urothelial cells in the late stage of BBN exposure. The studies also suggest that RhoGDIß may be a useful biomarker for evaluating the progression of human bladder cancers.