CHEMICO-BIOLOGICAL INTERACTIONS化学-生物相互作用
CHEMICO-BIOLOGICAL INTERACTIONS(英文缩写 CHEM-BIOL INTERACT),ISSN 0009-2797,eISSN 1872-7786,中文译名:化学-生物相互作用 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 5.168 | Q1 |
| 2022 | 5.100 | Q1 |
| 2023 | 4.700 | Q1 |
| 2024 | 5.400 | Q1 |
| 2025 | 5.200 | Q1 |
CHEMICO-BIOLOGICAL INTERACTIONS 最新收录文献
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1. Chronic tetracycline exposure resulted in VPS13 dysregulation, lipid accumulation, and physiological impairments in Drosophila melanogaster.
1. 慢性四环素暴露导致黑腹果蝇中VPS13失调、脂质积累和生理损伤PMID:日期:2026-10-04Antibiotics are widely detected in the environment due to their extensive use in medicine, aquaculture, and animal husbandry. Among these, tetracycline (TC) is recognized as a significant environmental contaminant with considerable ecological and public health implications. Continuous exposure to TC through contaminated food, water, and soil can lead to the accumulation of TC residues in the body, potentially exerting adverse effects on human health. To evaluate these effects, we used Drosophila melanogaster as a model organism. Our findings demonstrated that chronic exposure to TC at 1 mg/ml disrupted both metabolic and endocrine homeostasis as indicated by altered prothoracic gland morphology, reduced expression of ecdysone biosynthetic genes spo, phm, and dib, and significantly decreased 20-hydroxyecdysone levels. These changes were associated with developmental delay and reduced fecundity. TC exposure also increased lipid droplet accumulation, elevated TAG and glucose levels, shortened lifespan, and impaired locomotion. In addition, TC-treated flies exhibited reduced VPS13 expression, mitochondrial fragmentation, increased expression of Drp1, Pink1, Parkin, and Atg8a, enhanced oxidative stress, diminished antioxidant defences, and increased apoptosis. Molecular docking and molecular dynamics simulations further suggested a potential interaction between TC and the lipid-binding region of VPS13. Collectively, these findings indicate that chronic TC exposure is associated with altered lipid and endocrine homeostasis, mitochondrial dysfunction, oxidative stress, and impaired physiological performance in D. melanogaster. The observed reduction in VPS13 expression, together with the computational interaction analyses, suggests that VPS13 may contribute to the biological responses associated with TC exposure; however, further experimental studies are required to establish a direct mechanistic relationship.
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2. Zinc Deficiency Exacerbates Cisplatin-Induced Acute Kidney Injury by Impairing Metabolic Adaptation and Antioxidant Defenses.
2. 锌缺乏通过损害代谢适应和抗氧化防御加重顺铂诱导的急性肾损伤PMID:日期:2026-10-03Cisplatin-induced acute kidney injury (Cis-AKI) is a major limitation of chemotherapy and is largely driven by the inability of renal tubular epithelial cells to adapt to metabolic and oxidative stress. Zinc, an essential regulator of cellular stress responses, may influence this vulnerability, but its role in cisplatin nephrotoxicity remains unclear. Here, zinc-normal and zinc-deficient mice were subjected to Cis-AKI. Renal injury was evaluated by histology, serum creatinine (Scr), blood urea nitrogen (BUN), renal zinc levels, and NGAL expression. Transcriptomic analysis was performed to identify pathways altered by zinc deficiency, followed by validation of the AMPK/SIRT1/PGC-1α axis. Oxidative stress and apoptosis were assessed by Nrf2 signaling, antioxidant enzyme expression, SOD activity, MDA levels, TUNEL staining, and Bax/Bcl-2 expression. Zinc deficiency significantly aggravated Cis-AKI, as indicated by increased tubular damage, elevated Scr, BUN, and NGAL levels, and reduced renal zinc content. RNA sequencing revealed suppression of energy metabolism-related programs, accompanied by inhibition of the AMPK/SIRT1/PGC-1α axis, suggesting impaired metabolic adaptation. Zinc deficiency was also associated with reduced Nrf2 signaling, accompanied by decreased expression of antioxidant enzymes and total SOD activity, increased MDA accumulation, and enhanced tubular apoptosis. These findings suggest that zinc deficiency exacerbates Cis-AKI by weakening metabolic adaptation and antioxidant defenses, thereby promoting oxidative stress and apoptosis. Our study identifies zinc as a key regulator of tubular stress adaptation and suggests zinc homeostasis as a potential therapeutic target in cisplatin nephrotoxicity.
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3. Chemical proteomic identification of STUB1 as a direct target of benzophenone-3 reveals disrupted NRF2 signaling in chondrocytes.
3. 化学蛋白质组学鉴定STUB1为二苯酮-3的直接靶点揭示软骨细胞中NRF2信号通路受到破坏PMID:日期:2026-10-03Osteoarthritis (OA) is a common age-related degenerative joint disease, and emerging evidence implicates environmental chemical exposures as potential contributors. Benzophenone-3 (BP-3), a widely used ultraviolet filter frequently detected in human biospecimens, has been associated with increased OA risk, yet its direct molecular targets and mechanisms of cartilage toxicity remain unclear. Here, we applied an alkyne-tagged BP-3 probe combined with click chemistry-enabled chemical proteomics (SILAC-ABPP), transcriptomics, network toxicology, and experimental validation to investigate the molecular mechanisms underlying BP-3-induced cartilage toxicity. SILAC-ABPP identified the E3 ubiquitin ligase STUB1 as a direct cellular target of BP-3, which was further supported by cellular thermal shift assays and LC-MS/MS analysis. BP-3 exposure significantly increased STUB1 expression both in vivo and in vitro. Network toxicology and transcriptomic integration further implicated NRF2 in the STUB1-associated response to BP-3. BP-3-induced suppression of NRF2 was substantially attenuated by STUB1 knockdown, supporting a functional relationship between STUB1 and NRF2 in the cellular response to BP-3. STUB1 knockdown also attenuated BP-3-induced extracellular matrix disruption and ferroptosis-associated alterations, whereas NRF2 deficiency further aggravated these stress responses in chondrocytes. Chronic BP-3 exposure in mice recapitulated key pathological changes, including increased MMP13 expression, loss of collagen II, and altered ferroptosis-associated markers in articular cartilage. Collectively, these findings identify STUB1 as a direct molecular target of BP-3 and implicate STUB1-associated disruption of NRF2-dependent antioxidant responses in BP-3-induced cartilage toxicity.
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4. Doxorubicin-induced cardiotoxicity: SESN2-directed FBXO7 ubiquitination of CRY1 restores glycolytic homeostasis.
4. 多柔比星诱导的心脏毒性：SESN2引导的FBXO7对CRY1的泛素化恢复糖酵解稳态PMID:日期:2026-10-01Doxorubicin (DOX), a cornerstone anthracycline antineoplastic agent, induces cumulative, dose-limiting cardiotoxicity that remains a major barrier to its clinical use. Accumulating evidence suggests that maladaptive metabolic remodeling-particularly loss of glycolytic competence-contributes centrally to DOX-induced cardiac dysfunction. Here we identify Sestrin 2 (SESN2) as a cardiomyocyte-intrinsic metabolic safeguard that maintains glycolytic integrity under anthracycline stress. Integrative transcriptomic analyses reveal that SESN2 is suppressed in DOX-injured myocardium and is closely aligned with glycolytic gene programs. In murine models of acute and chronic cardiotoxicity, DOX reduces cardiac SESN2 expression concomitant with broad repression of glycolytic function; cardiomyocyte-restricted Sesn2 overexpression restores glycolytic activity, dampens inflammation, and oxidative stress, and preserves systolic function, whereas Sesn2 depletion precipitates glycolytic collapse and exacerbates cardiac dysfunction. Mechanistically, we define cryptochrome 1 (CRY1) as a critical downstream effector of SESN2-driven metabolic control. SESN2 directly associates with CRY1 and promotes FBXO7-dependent ubiquitination at Lys159, accelerating proteasomal degradation of CRY1 and thereby derepressing glycolytic programs. Consistently, cardiac Cry1 knockdown rescues glycolytic defects and functional decline elicited by Sesn2 loss in vivo. Together, these findings establish a SESN2-FBXO7-CRY1 proteostasis-metabolism axis that links anthracycline chemical stress to glycolytic failure and nominate SESN2-centered interventions as a rational strategy to restore myocardial metabolic homeostasis and mitigate DOX cardiomyopathy.
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5. Integrated network toxicology, machine learning, and multi-omics characterization of 2,4-DTBP neurotoxicity.
5. 整合网络毒理学、机器学习和多组学对2,4-DTBP神经毒性的表征PMID:日期:2026-10-012,4-Di-tert-butylphenol (2,4-DTBP) is an emerging alkylphenol antioxidant with potential neurotoxicity concerns, but its molecular toxicological basis remains poorly defined. Here, we applied an integrated framework combining network toxicology, machine learning-assisted target prioritization, molecular docking, cellular validation, and integrated transcriptomic-metabolomic profiling to delineate 2,4-DTBP-induced neurotoxic mechanisms. Network toxicology implicated PI3K/AKT, MAPK, calcium signaling, cytokine-cytokine receptor interaction, and ATP-binding cassette (ABC) transporter pathways as major 2,4-DTBP-associated axes. By integrating three machine learning algorithms including least absolute shrinkage and selection operator (LASSO) regression, support vector machine-recursive feature elimination (SVM-RFE), and random forest (RF), we convergently prioritized six candidate genes potentially associated with 2,4-DTBP-related neurotoxicity: Erb-B2 receptor tyrosine kinase 2 (ERBB2), colony-stimulating factor 1 receptor (CSF1R), RET proto-oncogene (RET), C-C motif chemokine ligand 22 (CCL22), ATP-binding cassette subfamily C member 5 (ABCC5), and ATP-binding cassette subfamily C member 1 (ABCC1). SHapley Additive exPlanations (SHAP) quantified their contributions and improved model interpretability, while molecular docking provided preliminary structural insights into the potential interactions between 2,4-DTBP and its corresponding target proteins. In SH-SY5Y cells, 100 μM 2,4-DTBP exposure elicited pronounced cytotoxicity characterized by oxidative stress, mitochondrial alterations, lipid peroxidation, intracellular iron accumulation, apoptosis, ferroptosis-related perturbations, and pronounced inflammatory responses. Western blotting further confirmed alterations in the phosphorylation levels of AKT, ERK, NF-κB p65, and CaMKII. Ferrostatin-1 mitigated the 2,4-DTBP-induced reduction in cell viability, oxidative stress, mitochondrial dysfunction, lipid peroxidation, Fe accumulation, and cell death, while partially restoring the transcriptional changes in GPX4, SLC7A11, GCH1, and ACSL4. Multi-omics integration further revealed coordinated disruption of inflammatory programs, synapse-related pathways, amino acid and energy metabolism, and redox homeostasis. Collectively, these results support a multi-level mechanistic framework for understanding 2,4-DTBP-induced neurotoxicity and identify candidate molecular targets and potential biomarkers for assessing the environmental neurotoxicity risks of emerging phenolic contaminants.
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6. MtROS-Drp1-mediated mitochondria fission contributes to microglia BV2 cell apoptosis induced by titanium dioxide nanoparticles.
6. MtROS-Drp1介导的线粒体裂变参与二氧化钛纳米颗粒诱导的小胶质细胞BV2细胞凋亡PMID:日期:2026-09-30The widespread use of titanium dioxide nanoparticles (TiO NPs) has raised serious concerns regarding their biosafety, particularly their potential effects on the central nervous system. As innate immune cells in the brain, microglia serve as key targets for neurotoxicity assessment. This study aims to systematically elucidate the toxic effects of TiO NPs on BV2 cells and their underlying molecular mechanisms. The results showed that TiO NPs were spherical, with an average particle size of approximately 10 nm, and primarily existed in the anatase phase. TiO NPs significantly inhibited BV2 cell viability in a concentration-dependent manner and induced apoptosis as well as autophagosome formation. Mechanistically, TiO NPs exposure triggered mitochondrial network fragmentation, membrane depolarization, and bursts of both intracellular and mitochondrial ROS. Notably, the mitochondrial-targeted antioxidant mito-TEMPO effectively attenuated these deleterious effects. Western blot analysis further revealed that TiO NPs activated the mitochondria-dependent apoptotic pathway, upregulated the mitochondrial fission protein Drp1, downregulated the fusion protein OPA1, and promoted autophagic flux. Metabolomic analysis identified 206 significantly differentially expressed metabolites, primarily enriched in pathways such as the tricarboxylic acid cycle, glutamine metabolism, glutathione metabolism, and purine metabolism, revealing the metabolic basis of energy metabolism disruption and exacerbated oxidative stress. In summary, these findings demonstrate that TiO NPs induce oxidative stress, which drives mitochondrial dynamic imbalance (fission/fusion disruption) and dysfunction, subsequently triggering metabolic reprogramming, apoptosis, and autophagy in BV2 cells. This study provides important experimental evidence and novel mechanistic insights into the neurotoxic potential of TiO NPs.
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7. The emerging contaminant HFPO-TA impairs hepatic glucose metabolism and induces pparγ-associated lipid metabolic disorders in zebrafish.
7. 新兴污染物HFPO-TA损害斑马鱼肝脏葡萄糖代谢并诱导pparγ相关脂质代谢紊乱PMID:日期:2026-09-30Hexafluoropropylene oxide trimer acid (HFPO-TA) is a new alternative to PFOA; it is already widely used and has caused global pollution. Previous studies have suggested that HFPO-TA may influence hepatic glucose and lipid metabolism via PPAR signaling pathway, however, the underlying molecular mechanism remains unclear. Here, a model of pparγ-knockout (pparγ-KO) zebrafish was used to investigate the mechanisms involving the disorders of glucose and lipid metabolism in the liver induced by HFPO-TA. In this study, a range of techniques were employed, including pparγ-KO (pparγ) zebrafish, transgenic zebrafish, histological staining, biochemical assays, fluorescence quantitative PCR, and transcriptomics. Zebrafish were exposed to HFPO-TA at concentrations of 1.25, 5 and 20 μM for 72 h post-exposure (hpe). The results indicated that exposure to HFPO-TA induced hepatomegaly, neutrophilic infiltration and hepatic lipid accumulation, accompanied by significantly elevated total cholesterol (TC) and triglyceride (TG) levels. In addition, exposure to HFPO-TA was associated with reduced glucose uptake and hepatic glycogen synthesis (as evidenced by downregulated expression of gys2). Using pparγ-KO zebrafish, we found that pparγ knockout attenuated HFPO-TA-induced lipid accumulation and reduced TC and TG elevations, but further exacerbated the inhibition of glucose uptake and glycogen synthesis. pparγ activation was associated with lipid metabolism disorders in the livers of zebrafish, correlating with increased lipid accumulation and liver damage. Collectively, these results reveal that HFPO-TA activates pparγ signaling to induce lipid metabolic disorders, providing important insights for risk assessment of metabolic diseases associated with environmental pollutants.
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8. 4-Nerolidylcatechol binds to Derlin-1 and modulates endoplasmic reticulum stress markers of androgen-independent prostate cancer cells.
8. 4-橙花基儿茶酚与Derlin-1结合并调节雄激素非依赖性前列腺癌细胞的内质网应激标志物PMID:日期:2026-09-29Castration-resistant prostate cancer (CRPC) is a lethal disease characterized by androgen receptor-independent activation mechanisms that promote prolonged or unresolved endoplasmic reticulum (ER) stress. Consequently, these cells rely on the endoplasmic reticulum-associated degradation (ERAD) pathway, specifically Derlin-1, to maintain proteostasis under chronic stress, which makes this protein a significant therapeutic target. We previously demonstrated that 4-Nerolidylcatechol (4-NC), the main secondary metabolite of Piper umbellatum (capeba), downregulates the epithelial-mesenchymal transition in androgen-independent prostate cancer cells (PC-3). In this study, we aimed to evaluate the potential of 4-NC to interact with Derlin-1 and modulate redox status and ER stress markers using in silico and in vitro approaches. Docking simulations and 100-ns molecular dynamics predicted that 4-NC binds within the Derlin-1 retrotranslocation channel, establishing polar interactions with Arg85 and Thr88 and hydrophobic contacts with Val142, Met140, Ala152, and Leu155, thereby conferring conformational stability to the complex in silico. In PC-3 cells, 4-NC exhibited concentration-dependent cytotoxicity and antiproliferative selectivity, with IC values of 39.2 μM in PC-3 and 86.7 μM in non-neoplastic PNT-2 cells (SRB assay; p < 0.05). Functional assays showed that 4-NC, at sub-cytotoxic concentrations, significantly increased intracellular reactive oxygen species levels, reduced glutathione levels by up to approximately 70%, enhanced lipid peroxidation, and progressively induced mitochondrial depolarization in PC-3 cells (p < 0.05). Consistently, 4-NC induced the expression of transcripts related to UPR/ERAD pathways (ATF4, BiP, EDEM, CHOP) and altered the proteome of treated PC-3 cells, indicating the activation of ER stress responses and a shift toward a pro-apoptotic transcriptional profile at higher concentrations. These findings highlight 4-NC as a promising natural compound for targeting the Derlin-1/ERAD axis, shedding light on mechanisms and promising targets not yet described in CRPC. Although previous reports demonstrated that 4-NC regulates the epithelial-mesenchymal transition in PC-3 cells, the present study identified, for the first time, Derlin-1 as a potential molecular target of 4-NC, highlighting the role of ER stress in CRPC.
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9. Prenatal exposure to perfluorooctane sulfonate and the risk of neurodevelopmental disorders: Perturbation of placenta-brain axis through DNA methylation.
9. 产前全氟辛烷磺酸暴露与神经发育障碍风险：通过DNA甲基化扰动胎盘-脑轴PMID:日期:2026-09-28Per- and poly-fluoroalkyl substances (PFAS) have been increasingly associated with adverse neurodevelopmental outcomes. The placenta serves as a critical interface between the maternal environment and fetal brain development; however, the epigenetic mechanisms underlying the association between prenatal PFAS exposure and neurodevelopmental outcomes remain poorly understood. In this study, we investigated whether maternal exposure to perfluorooctane sulfonate (PFOS) was associated with placental DNA methylation alterations and early-life neurodevelopmental outcomes through a potential placenta-brain axis. Using mother-infant pairs selected from the Shanghai Birth Cohort (SBC), we performed whole-genome DNA methylation profiling on placental samples and found that maternal PFOS levels were inversely associated with cognitive scores at 24 months. PFOS exposure was associated with widespread alterations in the placental methylome, with differentially methylated regions (DMRs) enriched in genes involved in neurodevelopmental processes. Among these, MDGA1, AR, DCC, NFASC, ATP9A, and ADAMTS19 were prioritized as candidate genes based on differential methylation patterns and network-based analyses, and their methylation alterations showed associations with both maternal PFOS exposure and offspring cognitive performance. These candidate epigenetic alterations were further examined in a prenatal PFOS-exposed rat model, in which changes in placental DNA methylation were accompanied by impairments in offspring spatial learning and memory. Collectively, our findings suggest that placental epigenetic dysregulation may represent a potential molecular link between prenatal PFOS exposure and early-life neurodevelopmental outcomes, highlighting the placenta-brain axis as a sensitive target of environmental exposure and providing candidate biomarkers for future investigation.
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10. Chloroxylenol induces hematopoietic bias and immune dysregulation in zebrafish associated with MAPK signaling disruption.
10. 氯二甲酚通过干扰MAPK信号通路诱导斑马鱼造血偏倚和免疫失调PMID:日期:2026-09-23Chloroxylenol (PCMX), a widely used phenolic disinfectant, is an emerging aquatic pollutant whose immunotoxicity remains poorly understood. This study employed zebrafish models to evaluate PCMX toxicity across a concentration range (0.25-7.5 mg/L) spanning environmentally detectable levels to higher, toxicologically informative concentrations. Acute exposure caused dose-dependent developmental defects, oxidative stress, and apoptosis in both embryos and adults. Embryonic toxicological assessment revealed a 96-h LC of 3.98 mg/L for larvae, with significant hatching reduction at ≥2 mg/L and malformation elevation at ≥0.5 mg/L. PCMX disrupted innate immunity by depleting neutrophils while paradoxically expanding macrophages, RNA-seq revealed 353 dysregulated genes in adult kidney, with KEGG enrichment identifying the MAPK pathway as a central hub. Network toxicology and molecular docking predicted moderate binding of PCMX to MAPK nodes (TGFBR1, GRB2, AKT1; -6.66 to -4.5 kcal/mol), corroborated by qPCR validation of MAPK and hematopoietic regulators (optn, atf3, irak3, prkcba, tgfbr2a, spi1a, c1qb, fosab). We propose that PCMX-induced oxidative stress converges on MAPK disruption, driving immune dysregulation and biased hematopoiesis, though this causal model is inferred from correlative evidence and requires functional validation. Despite the concentration gap, these findings show that PCMX, even at sublethal doses, can disrupt conserved immune and hematopoietic pathways, raising concern for aquatic organisms.