Are silymarin and N-acetylcysteine able to prevent liver damage mediated by multiple factors? Findings against ethanol plus LPS-induced liver injury in mice.

This study investigated the effect of N-acetylcysteine (NAC) and silymarin (SIL) in the liver of mice exposed to ethanol and lipopolysaccharides (LPS). Mice were divided into four groups (n = 6): naive, vehicle, NAC (200 mg/kg), and SIL (200 mg/kg). Treatments were given orally (po) once daily for 10 days. Liver injury was induced by administration of ethanol (30%, po) for 10 days, once daily, followed by a single administration of LPS (2 mg/kg, ip) 24 h before euthanasia. After the treatment period, animals were euthanized, and liver and blood samples were collected. NAC, but not SIL, prevented the increase in oxalacetic glutamic transaminase (OGT) and pyruvic glutamic transaminase (PGT) serum levels. NAC and SIL did not restore levels of reduced glutathione or hepatic malonaldehyde. The treatments with NAC or SIL showed no difference in the activity of glutathione S-transferase, superoxide dismutase, and catalase compared to vehicle group. Myeloperoxidase and N-acetylglucosaminidase activities are increased, as well as the IL-6 and IL-10 levels in the liver. The treatment with NAC, but not SIL, reduced the N-acetylglucosamines activity and the IL-6 and IL-10 amount in the liver. Histological findings revealed microsteatosis in the vehicle group, which was not prevented by SIL but was partially reduced in animals receiving NAC. Unlike other liver injury models, NAC (200 mg/kg) or SIL (200 mg/kg) did not positively affect antioxidant patterns in liver tissue of animals exposed to ethanol plus LPS, but NAC treatment displays anti-inflammatory properties in this model.

Comparison of oral cavity protein abundance among caries-free and caries-affected individuals-a systematic review and meta-analysis.

Objective: Some salivary proteins seem to be differently abundant among caries-free (CF) and caries-affected (CA) individuals, but previous results are contradictory precluding that definitive conclusion be drawn. A pooled analysis of the available evidence may provide more robust data on identifying oral cavity protein patterns among CF and CA individuals. This systematic review and meta-analysis (PROSPERO CRD42021269079) aimed to compare the oral cavity protein abundance among caries-free and caries-affected individuals. Methods: This study was conducted following PRISMA guidelines. PubMed, Embase, and Web of Science databases were systematically assessed (up to February 2023) to retrieve clinical studies written in English, German, or in Latin-based languages that compared the oral cavity protein abundance among CF and CA individuals. Data extraction and methodological quality assessment (NIH guidelines) were independently performed by two investigators. Qualitative synthesis was performed from all included studies and meta-analysis was performed using a random-effects model with inverse variance for studies that reported the concentration of proteins or enzymatic activity. Standardized mean difference (SMD) with respective 95% confidence interval (CI) were calculated for each outcome. Results: A total of 90 studies (two cohort and 88 cross-sectional designs) of more than 6,000 participants were selected for data extraction, being the quality of evidence graded as "fair" for most of them. The oral cavity of CF individuals presented lower total protein concentration [SMD = 0.37 (95% CI: 0.07-0.68; 18 studies)], lower total antioxidant capacity [SMD = 1.29 (95% CI: 0.74-1.85); 17 studies], and lower carbonic anhydrase activity [SMD = 0.83 (95% CI: 0.58-1.09); three studies], whereas CA individuals presented lower carbonic anhydrase concentration [SMD = -0.66 (95% CI: -1.00 to -0.32); three studies], urease [SMD = -0.95 (IC 95%: -1.72 to -0.17); four studies], and arginine deiminase system [SMD = -2.07 (95% CI: -3.53 to -0.62); three studies] activities. Antimicrobial peptides, secretory immunoglobulin-A concentrations and alpha-amylase activity were similar among individuals. Conclusion: Differences on oral cavity protein abundance were observed among CF and CA individuals. These data indicate some protein patterns for the oral health and dental caries conditions. Even when statistically significant, some of the results were not very consistent. Cohort studies need to be conducted to validate these results.

A new in vitro study demonstrates that electronic cigarettes promote cellular carcinogenic characteristics.

Electronic cigarettes have been used as a new form of cigarettes, especially among young people, but the impact of these effects on mouth cancer is unknown. Therefore, there is a need for studies to evaluate their impact on health and oral mucosa. In this way, this study evaluates the risk of electronic cigarette liquid on in vitro cells of a panel: normal oral epithelium cell lines (NOE and HMK), oral squamous cell carcinoma human cell lines (CAL27 and HSC3), and a mouse oral cancer cell line (AT84). It was demonstrated that electronic cigarettes promote proliferation and anchorage-independent growth and induces morphological changes associated with enhanced motility and invasive phenotypes. Also, it was observed that the enhanced invasive migratory activity associated with the loss of epithelial markers, such as E-cadherin, and the acquisition of mesenchymal markers, strongly suggest that epithelial cells are undergoing to an aggressive phenotype within the framework of epithelial-mesenchymal transition. In conclusion, the liquid can promote carcinogenesis, in addition to promoting an aggressive phenotype in pre-existing lesions.

Does periodontal disease have an association with prostate cancer?

Data sources The electronic databases PubMed, Embase and the Cochrane Oral Health Group's Trials Register up to 7 July 2020 were searched to identify eligible studies. Information sources in the grey literature were not cited.Study selection Cohort studies and case-control studies in English were selected by two reviewers independently. All articles had to include a control patient group (without periodontal disease) and a group with periodontal disease and both groups with prostate cancer outcomes. Also, all articles reported the hazard ratio (HR), relative risk (RR) or odds ratio (OR) estimates with their 95% confidence intervals (CIs).Data extraction and synthesis Data extraction and risk of bias assessments were performed by two reviewers independently and any disagreements between these authors were resolved through discussion or by consulting a third author. Data were synthesised qualitatively by the Newcastle-Ottawa Scale. RR with 95% CI was used as the pooled estimate to assess the association of periodontal disease and the risk of prostate cancer. When the outcome of interest was rare, it was considered that the OR approximated the RR (24). HR was also treated as RR when pooled in this meta-analysis. The heterogeneity across studies was evaluated by Q test (statistical significance was considered when P <0.1) and the I2 statistic (I2 ≥50% indicated significant heterogeneity).Results Seven studies were included in the meta-analyses, with four being prospective cohort studies and three retrospective cohort studies. All studies were of high quality except one study that was considered to be of moderate quality. Pooled estimates indicated that periodontal disease had a significant statistical relationship with the risk of prostate cancer (RR = 1.17; 95% CI = 1.07-1.27; P = 0.001). No significant heterogeneity across studies was observed (P = 0.383; I2 = 5.8%). The studies include Asian, European and American populations.Conclusions The authors of this review concluded that periodontal disease could be a possible risk for prostate cancer and that the male public, and clinicians, should be aware of the importance of maintaining good periodontal health.