Pesticide exposure has deleterious effects on human health and development; however, no review has been conducted on human exposure to pesticides and the risk of congenital malformations and cancer in the same cohort. We systematically reviewed the evidence for this relationship following the Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines. Four databases, namely, PubMed, Scopus, Cochrane Library, and BVS, were searched for studies deposited till July 2020 that examined the influence of pesticide exposure on congenital malformations and cancer outcomes in the same cohort. Seven studies were systematically included in this review. Among these, four were case–control studies, two were cross-sectional studies, and one was a longitudinal cohort study. The sources of contamination were food, water, or exposure during agricultural work. A link between the occurrence of cancer, congenital malformations, and exposure to pesticides was observed in most studies.

Triple-negative breast cancer (TNBC) is an aggressive, fast-growing tumor that is more likely to spread to distant organs. Among women diagnosed with breast cancer, the prevalence of TNBC is 20%, and treatment is currently limited to chemotherapy. Selenium (Se), an essential micronutrient, has been explored as an antiproliferative agent. Therefore, this study aimed to evaluate the effects of exposure to organic (selenomethionine, ebselen, and diphenyl diselenide) and inorganic (sodium selenate and sodium selenite) Se molecules in different breast cell lines. The compounds were tested at 1, 10, 50, and 100 μM for 48 h in the non-tumor breast cell line (MCF-10A) and TNBC derivatives cell lines (BT-549 and MDA-MB-231). The effects of Se on cell viability, apoptotic and necrotic processes, colony formation, and cell migration were analyzed. Exposure to selenomethionine and selenate did not alter the evaluated parameters. However, selenomethionine had the highest selectivity index (SI). The exposure to the highest doses of selenite, ebselen, and diphenyl diselenide resulted in antiproliferative and antimetastatic effects. Selenite had a high SI to the BT cell line; however, the SI of ebselen and diphenyl diselenide was low in both tumoral cell lines. In conclusion, the Se compounds had different effects on the breast cell lines, and additional tests are needed to reveal the antiproliferative effects of Se compounds.

Background: Ganoderma lucidum triterpenes are bioactive compounds with recognized anti-inflammatory, antitumor, and immunomodulatory properties. This systematic review synthesizes evidence regarding the anti-inflammatory activity of these triterpenes based on studies from the last two decades. Methods: A systematic search was performed in PubMed, Medline, and Embase (2003–2025) for original in vitro and in vivo (non-clinical) studies evaluating G. lucidum triterpene extracts or isolated compounds. Clinical trials, reviews, and multi-species extracts were excluded. The review is registered on PROSPERO (CRD42024510982), and animal study quality was assessed using the SYRCLE Risk of Bias tool. Findings: From over 3000 records, 23 articles were included. Studies utilized diverse models, including macrophages, human PBMCs, and various animal strains (mice, rats, chickens). All studies reported significant anti-inflammatory effects via reduction in pro-inflammatory markers (TNF-α, IL-1β, IL-6), primarily through downregulation of MAPK and TLR-4/NF-κB signaling pathways. Meta-analysis of in vitro data confirmed significant reductions in NO levels (−3.29 [95% CI: −5.21, −1.37]; p = 0.0008), IL-6 (−3.51 [−4.73, −2.29]; p < 0.00001), and TNF-α (−2.20 [−2.93, −1.48]; p < 0.00001). Similar anti-inflammatory profiles were observed in vivo across hepatic and splenic tissues. Interpretation: Evidence consistently demonstrates the potent anti-inflammatory activity of G. lucidum triterpenes, highlighting their potential as therapeutic candidates for inflammatory diseases. However, the structural complexity and isomer diversity of these compounds remain significant barriers to pharmacological standardization. Future research must prioritize clinical translation by investigating compound synergism, bioavailability, and long-term toxicity profiles, which were notably absent in current non-clinical literature.

Opioid drugs have analgesic properties used to treat chronic and post-surgical pain due to descending pain modulation. The use of opioids is often associated with adverse effects or clinical issues. This study aimed to evaluate the toxicity of opioids by exposing the neuroblastoma cell line (SH-SY5Y) to 0, 1, 10, and 100 µM oxycodone and naloxone for 24 h. Analyses were carried out to evaluate cell cytotoxicity, identification of cell death, DNA damage, superoxide dismutase (SOD), glutathione S-transferase (GST), and acetylcholinesterase (AChE) activities, in addition to molecular docking. Oxycodone and naloxone exposure did not alter the SH-SY5Y cell viability. The exposure to 100 µM oxycodone and naloxone significantly increased the cells’ DNA damage score compared to the control group. Naloxone exposure significantly inhibited AChE, GST, and SOD activities, while oxycodone did not alter these enzymes’ activities. Molecular docking showed that naloxone and oxycodone interact with different amino acids in the studied enzymes, which may explain the differences in enzymatic inhibition. Naloxone altered the antioxidant defenses of SH-SY5Y cells, which may have caused DNA damage 24 h after the exposure. On the other hand, more studies are necessary to explain how oxycodone causes DNA damage.

Background: Opioids are commonly used to manage both acute and chronic pain by acting on opioid receptors in the central and peripheral nervous systems. However, concerns about their increasing prescription and misuse have emerged due to adverse effects, toxicity, and the global impact of opioid-related harm. Objectives: This systematic review aims to evaluate the harmful (adverse and toxic) effects of prescribed opioids on the pediatric and the general population. Methods: Following PRISMA guidelines, a systematic search was conducted for data from January 2011 to December 2024 across selected electronic databases (PubMed^®, SciELO^®, Web of Science^®, and EMBASE^®) using a specific search strategy with Boolean operators. Cross-sectional, cohort, and case–control designs published in English, analyzing and identifying the harmful effects of prescribed opioids in children and the general population, were eligible for inclusion. Three reviewers independently assessed titles and abstracts for eligibility, followed by a full-text review. A referee reviewer resolved discrepancies. Data extraction was performed for qualifying studies. The risk of bias was assessed by the ROBINS-I tool. Results: A total of 3984 papers were collected, with 1697 duplicates and 2062 non-eligible papers removed; resulting in 25 papers (112.825 patients) selected for qualitative analysis. The pediatric group experienced more harmful effects across multiple body systems (nausea and vomiting, hypotension, agitation, drowsiness/lethargy, lethargy, respiratory depression, aspiration pneumonia) compared to the general population (dominant S wave, long QTc interval, right axis deviation, seizure). Conclusions: Despite the data heterogeneity, this study highlights the importance of evaluating the harmful effects of opioids, particularly in pediatric patients, to assess the risk–benefit balance and health risks associated with their use. The lower number of effects in the general population may be attributed to increased pharmacological tolerance and tolerability.

Background/Objectives: Neuroblastoma is a pediatric embryonal tumor of the autonomic nervous system, characterized by high heterogeneity. Recent research has explored the therapeutic potential of retinoic acid and selenium derivatives as antiproliferative agents. This study aims to assess the antiproliferative effects of sodium selenite and retinoic acid, as well as the conventional chemotherapeutic agents, cyclophosphamide and cisplatin, using the SH-SY5Y neuroblastoma cell line. Methods: Cells were treated with the compounds at concentrations ranging from 0 to 1000 µM for 72 h. The following assays were performed: cell viability, clonogenic assay, cell migration, cell cycle analysis, and gene expression (BCL2 and BAX). Data were analyzed using the Kruskal–Wallis test followed by Dunn’s or the Mann–Whitney test (p < 0.05). IC₅₀ values were obtained from dose–response curves. Results: Sodium selenite (100–1000 µM) significantly reduced cell viability by more than 50% (IC₅₀: 166 µM at 72 h). Retinoic acid (300 µM) reduced viability by 65% (IC₅₀: 198 µM at 72 h), and cisplatin (10 µM) reduced viability by 79% (IC₅₀: 3.4 µM at 72 h). All compounds significantly decreased colony formation. Sodium selenite and retinoic acid induced arrest in the G0/G1 phase of the cell cycle. Gene expression analysis revealed downregulation of the BCL2 gene by all compounds and upregulation of BAX only by sodium selenite at IC₅₀ concentration. Conclusions: Sodium selenite and retinoic acid showed antiproliferative effects on neuroblastoma cells, suggesting their potential as adjuvant therapeutic agents. To reach this goal, we suggest further investigation of their mechanisms of action and evaluation of the combined strategies.