Toxicology and Industrial Health

Li, Junxian; Dai, Yiting; Huang, Hefei; Zhong, Yichen; Zhu, Lijin

doi: 10.1177/07482337251342903pmid: 40464221

Asbestos is classified as a class I carcinogen by the International Agency for Research on Cancer (IARC) because of its propensity to accumulate in the lungs and induce malignant tumors, including lung cancer and malignant mesothelioma. The objective of this study was to examine the inhibitory impact of miR-30d on the proliferation, migration, and invasion of chrysotile-transformed human pleural mesothelial cells (MeT-5A). The asbestos-transformed cell model was constructed using a chrysotile asbestos chronically exposed human pleural mesothelial cell line (MeT-5A). The expression level of miR-30d in the transfected cells was determined by qRT-PCR. Cell viability was assessed by CCK-8 assay. The apoptosis rate was evaluated by flow cytometry. The cell scratch assay and the Transwell assay were used to assess cell migration and invasion ability. It was observed that the expression level of miR-30d in Asb MeT-5A+miR-30d cells transfected with miR-30d mimics was markedly elevated in comparison to that in Asb MeT-5A+miR NC cells. Additionally, the cell viability in Asb MeT-5A+miR-30d cells was significantly diminished, while the level of apoptosis was markedly elevated in comparison to that in Asb MeT-5A+miR NC cells. The relative migration area was significantly lower in the Asb MeT-5A+miR-30d group than in the Asb MeT-5A+miR NC group. Furthermore, the number of migrated and invaded cells in the Asb MeT-5A+miR-30d group was significantly less than in the Asb MeT-5A+miR NC group. The findings suggest that miR-30d may suppress the proliferation, apoptosis, migration, and invasion of chrysotile-transformed pleural mesothelial cells.

Madu, Francis Ugochukwu; Iroha Akubugwo, Emmanuel; Ekwutosi Ogbulie, Toochukwu; Obinwa Uhegbu, Friday; Agoro, Eni-yimini Solomon; Ulunma Nwosu, Oluchi; Ugbonma Ugenyi, Assumpta; Ononogbo, Purity Chioma; Madu, Miracle Chinwenmeri

doi: 10.1177/07482337251349359

Zhou, Xiangning; Yu, Jingjing; Sun, Tianwei; Wang, Ying; Yao, Zhenyu; Gao, Ling

doi: 10.1177/07482337251349366pmid: 40503734

Ferroptosis, a form of programmed iron-dependent cell death, is associated with various liver pathologies. Recent studies have increasingly highlighted the crucial role of ferroptosis in liver function. This study aimed to explore the development of ferroptosis in liver diseases through bibliometric analysis. We retrieved the data from the Web of Science (WOS) Core Collection, then imported selected articles into VOSviewer, CiteSpace, and Microsoft Excel for knowledge mapping analysis. A total of 1,236 articles were included in this study, showing a steady increase in publications on ferroptosis in the liver over the past 11 years, with a significant surge in recent years. China emerged as a dominant contributor, accounting for 86% of global publications. Key institutions included Zhejiang University and Sun Yat-sen University. Zhang Feng from Nanjing Medical University was identified as the most prolific author. The journal Frontiers in Pharmacology published the most articles on this topic. High-frequency keywords included “ferroptosis,” “cell death,” “hepatocellular carcinoma,” “oxidative stress,” and “cancer.” Our analysis provides insight into the leading countries, institutions, authors, and journals and it highlights recent research hotspots. As an emerging research field, studies on ferroptosis in the liver focused primarily on molecular mechanisms, pathways, and treatment strategies. Hepatocellular carcinoma remains a primary focus within ferroptosis research in the liver. In the future, therapies targeting ferroptosis may offer promising avenues for liver disease treatment.

Sharma, Manisha; Rajawat, Neelu Kanwar

doi: 10.1177/07482337251350165pmid: 40492926

Nanoparticles (NPs 1–100 nm) play a vital role in medicine, food, and agriculture owing to their unique reactivity and size-dependent optical properties. There are growing concerns about health risks from exposure to engineered NPs. Among these, copper oxide nanoparticles (CuONPs) are an area of research because of their unique electronic, optical, and chemical properties. CuONPs can interact with biological systems, causing oxidative stress, inflammation, neurobehavioral changes, and other pathophysiological effects. This study evaluated the ability of a probiotic (Lactobacillus acidophilus) to prevent CuONP-treated neurotoxicity. In the present study, 24 animals were classified into four groups: control, probiotic (Lactobacillus acidophilus 6.42 mg/kg b.wt.), CuONPs-treated (80 mg/kg b.wt.), and co-administered CuONPs (80 mg/kg b.wt.) + Probiotic (6.42 mg/kg b.wt.). Neurotoxicity was assessed through behavioral tests, including open field, exploratory behavior, pole test, and grip strength tests. Levels of key neurotransmitters viz. acetylcholinesterase, dopamine, and serotonin were measured and histopathological analyses were performed. The CuONP-treated group displayed significant behavioral deficits, decreased neurotransmitter levels, and histopathological abnormalities. In contrast, co-administration of probiotic with CuONPs reduced these effects, as observed by normal behavioral parameters and neurotransmitter levels and improved histopathological architecture. These findings suggested that CuONPs caused neurotoxicity at the tested dose, but co-administration of probiotic effectively mitigated this toxicity. Hence, a probiotic is a promising preventative strategy against CuONP-induced neurotoxic effects.

Bidu, Nadielle Silva; Reis, Paulo Roberto de Veloso; Couto, Ricardo David; Fernandes, Bruno Jose Dumêt

doi: 10.1177/07482337251343397pmid: 40396308

Titanium dioxide (TiO2) is a white powder used in toothpaste, pharmaceuticals, sunscreen, food additives, cosmetics, paints, decontaminants, and photocatalysts. It is produced and used in the workplace in fine and ultrafine particle sizes. International organizations set occupational exposure limits for fine and ultrafine TiO2 particles. TiO2 has not been confirmed to have carcinogenicity in humans, with available assessment data being limited and inconclusive owing to nonspecific effects observed from TiO2 inhalation. The purpose of this toxicological alert is to encourage new studies to determine whether TiO2 is a human carcinogen. TiO2’s classification as a possible carcinogen was based on laboratory experiments that produced TiO2 particles with 30–60 nm diameters. These studies assessed the potential risk of exposure to TiO2 nanoparticles, which have diverse and atypical characteristics compared to those found in workplace settings. To date, there are no studies with sufficient data on the duration of pulmonary exposure to TiO2 nanoparticles with significantly relevant workplace associations. Extrapolating results from rodent studies with limited parameter controls do not provide an adequate (translational) assessment of the toxicity of TiO2 nanoparticles on the human respiratory system.