Arsenic exposure has been implicated in various malignancies, including head and neck cancers (HNCs). However, the association between arsenic exposure and HNC development remains unclear. This systematic review aimed to assess the relationship between arsenic exposure and the risk of developing HNCs. This study adhered to PRISMA guidelines. A systematic search of PubMed, Embase, Scopus, and Web of Science was conducted from inception to January 2025 to identify relevant studies. Observational studies reporting the association between arsenic and HNCs were included. Two independent reviewers performed study selection, data extraction, and risk of bias assessment using the NIH criteria. A total of 24 studies met the eligibility criteria, including 35,641 cases and 4,631 controls. The mean age of cases was 50.3 years, while controls had a mean age of 57.7 years. Nineteen studies assessed nasopharyngeal/laryngeal cancers, and 13 investigated oral cancers. Environmental/occupational arsenic exposure was reported in 14 studies, while 11 studies measured arsenic levels in biological samples. Geographical differences in exposure outcomes were observed, with significant associations reported in studies from Tunisia, Chile, Brazil, and Taiwan, while studies from the UK, Finland, and a multicenter European study found no significant relationship. Blood, hair, soil, and drinking water arsenic concentrations varied across studies, with inconsistent findings. The findings suggest a potential link between arsenic exposure and HNCs, particularly in regions with high environmental contamination. However, heterogeneity in exposure assessment and study design limits definitive conclusions. Further well-controlled studies are needed to clarify the association and underlying mechanisms.

Jadomycin B, produced by the soil bacterium Streptomyces venezuelae ISP5230, induces cytotoxicity in human breast cancer cells in vitro and has antitumoral effects in animal models. In models of multidrugresistant, triple-negative breast cancer, jadomycin B has shown promise as it is not a substrate of ABCB1 and ABCG2 drug efflux transporters. The generation of reactive oxygen species and inhibition of topoisomerases are potential mechanisms of jadomycin B-mediated DNA damage and apoptosis. However, the mechanisms of jadomycin B's anticancer activity have not been fully elucidated. By gradually exposing MDA-MB-231 triple-negative human breast cancer cells to jadomycin B, we hypothesized that resistance could be selected to further understand jadomycin B's pharmacological mechanisms. A 3-fold increase in the jadomycin B IC50 was observed in MDA-MB-231 cells exposed to increasing jadomycin B concentrations (0-3 mu M) over 7 months, herein 231-JB cells. The 231-JB cells were cross-resistant to jadomycin F and S but not to the comparator drugs mitoxantrone, doxorubicin, and SN-38. The 231-JB cells did not have increased mRNA expression of topoisomerase-2 nor ABCB1 and ABCG2. Cyclooxygenase-2 (COX-2) increased by 25-fold, but expression of prostaglandin E2 receptor 4 did not significantly change. Cotreatment with celecoxib (15-45 mu M), a COX-2 inhibitor, resensitized the 231-JB cells to jadomycin B (IC50 1/4 1.41 +/- 0.24 to 0.75 +/- 0.31 mu M vs 2.28 +/- 0.54 with 0 mu M celecoxib). To our knowledge, this work represents the first report of the involvement of COX-2 in jadomycin B activity in vitro, proving to be an exciting new target for the exploration of jadomycin B anticancer activity. Significance Statement: Cyclooxygenase-2 (COX-2), the rate-limiting enzyme in prostaglandin production, is associated with procancer signaling. COX-2, ABCB1, and ABCG2 overexpression are typically correlated in cancer, contributing to chemotherapy resistance. We observed increased COX-2, but not ABCG2 or

Asbestos is a silicate mineral that occurs naturally and is made up of flexible fibres that are resistant to heat, fire, and chemicals and do not conduct electricity. Both anthropogenic disturbance and natural weathering of asbestos-containing waste materials (ACWMs) can result in the emission of asbestos fibre dust, which when breathed, can cause asbestosis, a chronic lung illness that happens due to prolonged exposure of such fibre dust, and can cause 'mesothelioma' cancer. Although asbestos mining and its utilisation had been banned in many countries, there is still a significant issue of ACWMs disposal in the built environment and abandoned sites. It is neither practical nor economical to safely eliminate ACWMs from the built environment, and it is estimated that globally, 4 billion metric tonnes of ACWMs require safe management strategies. The toxicity of inhaled asbestos fibre relies on its surface properties, and in particular the distribution of iron, which serves a critical role in pathogenicity by forming reactive free radicals that damage DNA, thereby trigging cancer. Examining the usefulness of higher plants and microbes in the bioremediation of soil contaminated with ACWMs is the prime aim of the review. Higher plants and microorganisms such as lichens, fungi, and bacteria often play a major role in the remediation of soil contaminated with ACWMs by facilitating the bioweathering of asbestos and the removal of iron to mitigate the toxicity of asbestos.

Heavy metal(loid)s (HM) pollution in aquatic environments is a serious issue due to the toxicity, persistence, bioaccumulation, and biomagnification of these pollutants. The main sources of HM contamination are industrial activities, mining, agricultural practices, and combustion of fossil fuels. Fish can accumulate HMs through a process called bioaccumulation. As larger predatory fish consume smaller fish, these HMs enter the main food chains and can become increasingly concentrated in their tissues and finally reach humans. Here, we provided a general and concise conclusion from current research findings on the toxicological effects on different body systems. Exposure to HMs can lead to a range of adverse health effects, including neurological damage, developmental disorders, kidney damage, cardiovascular problems, and cancers. Their long-term accumulation can result in chronic toxicity even at low levels of exposure. HMs exert cellular cytotoxicity by disrupting essential cellular processes and structures. They can interfere with enzyme function, disrupt cell membrane integrity, induce oxidative stress, and cause DNA damage, ultimately leading to cell death or dysfunction. Prevention and control of HMs involve implementing measures to reduce their release into the environment through regulations on industrial processes, waste management, and pollution control technologies. Additionally, monitoring and remediation efforts are crucial for identifying contaminated sites and implementing strategies such as soil and water remediation to reduce human exposure and mitigate the impact on ecosystems. To conclude, HM accumulation in fish poses serious risks to public health and the environment, necessitating urgent interdisciplinary efforts to mitigate their harmful effects and promote sustainable practices that reduce HM flow into biological systems.

Genotoxic agents are substances that can induce DNA damage; this damage can be caused by chemical, biological, and physical agents. The dose, time and route of exposure, and the genetic constitution of the individual influence the capacity of these agents to induce damage and may also be related to lifestyle habits and place of residency. Directly associated with genotoxicity is epigenetics, which is the study of hereditary changes in the function of hereditary genes not attributed to alterations in the DNA sequence. These processes regulate the expression of genes through the modulation of chromatin structure. The interaction of genetic and non-genetic factors in the control of hereditary patterns of this expression may cause diseases or disorders such as cancer, infertility, inflammatory processes, degenerative diseases, and endocrine disruption that could be transmitted to the offspring. Several epidemiological studies have shown that changes in lifestyle and eating habits could prevent or reduce cancer incidence; particularly by increasing the level of antioxidants and reducing the formation of free radicals with intracellular effects. At the Biotechnology Research Center of the Technological Institute of Costa Rica, various genotoxic agents to which the population in Costa Rica is exposed are investigated, including bacteria such as Helicobacter pylori, micro plastics in marine species for human consumption, and heavy metals in drinking water and in soils. These investigations are relevant to determine the presence of these genotoxic agents in the country, to evaluate the risk of exposure of the population, and thus generate strategies for prevention and mitigation of the damage.

The recent emergence of drug-resistant microorganisms and the prevalence of cancer diseases are both presenting substantial global public health concerns. Silver nanoparticles (AgNPs) have attracted significant attention and are increasingly employed in diverse biomedical applications as agents with antimicrobial and anticancer properties. The study herein focused on the biogenic synthesis of AgNPs employing the cell-free filtrate of the soil-derived bacterium Streptomyces pratensis as a reducing agent. AgNPs were characterized using UV-Vis, FTIR, FE-SEM, and TEM. The study assessed both the antibacterial and anticandidal modes of action, along with the potential anticancer properties of the biosynthesized AgNPs. The spherical, 17-44-nm biosynthesized AgNPs demonstrated strong antimicrobial and antibiofilm activities against pandrug-resistant (PDR) Gram-negative Klebsiella pneumoniae and pathogenic yeast Candida albicans, both of which were isolated from immunosuppressed patients. Dose-dependent interactions between the AgNPs and their anticancer activity were observed. The IC50 values of the AgNPs against the hepatocellular (HepG2) and colon carcinoma (HCT-116) cancer cell lines were approximately 16.5 mu g/mL and 11.5 mu g/mL, respectively. Furthermore, the antimicrobial mechanism of action of AgNPs revealed distinct leakage of sugar, DNA, and proteins from the cell membrane of both K. pneumoniae and C. albicans, as well as increased ROS generation. Moreover, the TEM micrographs depicted the distortion and damage experienced by the microbial cells after exposure to AgNPs. The findings of the current study suggest that biosynthesized AgNPs have the potential to serve as alternative therapeutic agents for combating drug-resistant K. pneumoniae, the yeast C. albicans, in addition to HepG2 and HCT-116 cells.

Breast cancer is one of the most common and deadly cancers in women worldwide. Current treatments for breast cancer have limitations, such as toxicity, resistance, and side effects. Therefore, there is a need to develop new and effective anti-cancer agents from natural sources. Spinosyn A (SPA) is a natural product derived from soil bacteria. SPA has been reported to have anti-parasitic, insecticidal, and anti-bacterial activities. However, its anti-cancer effects and mechanisms are not well understood. In this study, we investigated the effects of SPA on T47-D, estrogen receptor-positive breast cancer cells. We found that SPA inhibited cell proliferation and migration and induced apoptosis and cell cycle arrest. Flow cytometry and holographic imaging microscopy revealed that SPA activated MAPK and PI3K signaling pathways and altered cellular morphology. Finally, RNASeq analysis revealed that SPA treatment altered the expression of 1380 genes in T47-D cells, which were enriched in various biological processes and signaling pathways related to cell proliferation, cholesterol metabolism, growth factor activity, amino acid transport activity, extracellular matrix, PI3K-Akt signaling pathway, neuroactive ligand-receptor interaction, and PPAR signaling pathway. Our results suggest that SPA exerts multiple anti-cancer effects on T47-D cells by modulating multiple pathways and cellular processes involved in cell growth, survival, and motility. Our findings provide new insights into the molecular mechanisms of SPA action on breast cancer cells and its potential applications as a novel anti-cancer agent.

The genus Arthrobacter is a source of many natural products that are critical in the development of new medicines. Here, we isolated a novel carotenoid from Arthrobacter sp. QL17 and characterized its properties. The carotenoid was extracted with methanol, and purified by column chromatography and semi-preparative HPLC. Based on micrOTOF-Q and NMR analyses, the pigment was chemically characterized as 2,2 '-((((1E,3E,5E,7E,9E,11E,13E,15E,17E,19E)-3,7,14,18-tetramethylicosa-1,3,5,7,9,11,13,15,17,19-decaene-1,20-diyl)bis(2,2,4-trimethylcyclohex-3-ene-3,1-diyl)) bis(ethan-2-yl-1-ylidene))bi(propane-1,3-diol), and named arthroxanthin. The biological activities of arthroxanthin were evaluated with DPPH, ABTS and MTT assays. Arthroxanthin exhibited excellent radical scavenging properties, as shown for 2, 20-diphenyl-1-picrylhydrazyl (DPPH) and 2,2-n-(3,2-ethyl-benzothiazole-6-sulfonic acid) ammonium salt (ABTS), respectively, with IC50s of 69.8 and 21.5 mu g/mL. It also showed moderate anticancer activities against HepG2, Hela, MDAB-231, SW480, and MKN-45 with IC50 values of 107.6, 150.4, 143.4, 195.9, and 145.5 mu g/mL, respectively. Therefore, arthroxanthin derived from Arthrobacter sp. QL17 may be a potent antioxidant and anticancer agent for food and pharmaceutical use.