Environmental Toxicology最新文献

{"title":"Coleus vettiveroides Root Extract Protects Against Thioacetamide‐Induced Chronic Liver Injury by Inhibiting NF‐κB Signaling Pathway","authors":"Kadmad Abdul Hameed Mohamed Azar, Devaraj Ezhilarasan, Munusamy Karthick, Karthik Shree Harini, Venkatesan Kumar","doi":"10.1002/tox.24465","DOIUrl":"https://doi.org/10.1002/tox.24465","url":null,"abstract":"The roots of <jats:italic>Coleus vettiveroides</jats:italic> (CV) have been traditionally used in Indian medicinal systems such as Ayurveda and Siddha for its antioxidant, anti‐inflammatory, and antidiabetic effects. This study examines the antifibrotic potential of CV ethanolic root extract (CVERE) against thioacetamide (TAA)‐induced liver fibrosis in Wistar rats. TAA was administered via i.p., thrice weekly for 11 weeks to induce liver fibrosis in rats. In separate groups, rats were administered with TAA and were concurrently treated with CVERE 125 mg/kg, CVERE 250 mg/kg, and silymarin (SIL) 100 mg/kg. Liver marker enzymes of hepatotoxicity, oxidative stress markers, proinflammatory marker gene expression (TNF‐α, NF‐κB, COX, and ILs), fibrotic marker gene expression (collagen I and III), immune histochemical expression of fibrosis marker proteins, and histopathologic changes were analyzed. TAA administration led to a significant (<jats:italic>p</jats:italic> &lt; 0.001) increase in the serum level of hepatotoxic marker enzymes. The TAA‐treated group showed higher levels (<jats:italic>p</jats:italic> &lt; 0.001) of MDA and reduced activities of SOD and CAT in the liver. TAA administration increased CYP2E1 expression, proinflammatory, and fibrotic marker gene expressions in rat liver. The histopathology of the liver confirms TAA‐induced architectural distortion and fibrotic changes. CVERE and SIL simultaneous treatments significantly protected against TAA‐induced oxidative stress, inflammation, and liver fibrosis. In conclusion, CVERE inhibited TAA‐induced liver fibrosis through downregulation of TAA metabolic activation, redox imbalance, and inflammation through repression of the NF‐κB pathway.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"24 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142867280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Aluminum Oxide Nanoparticles in the Spinal Cord of Male Wistar Rats and the Potential Ameliorative Role of Melatonin","authors":"Nermeen G. Abdelhameed, Yasmine H. Ahmed, Noha A. E. Yasin, Mohamed Y. Mahmoud, Mohamed A. El‐sakhawy","doi":"10.1002/tox.24466","DOIUrl":"https://doi.org/10.1002/tox.24466","url":null,"abstract":"Aluminum oxide nanoparticles (Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> NPs) are widely utilized in vaccine manufacturing and other medical preparations. Melatonin has numerous effects as an antioxidant and anti‐apoptotic. The purpose of this study was to examine the beneficial impact of melatonin on Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> NPs toxicity in the spinal cord. Forty male rats were divided into four groups: Group I, the negative controls (received standard diet and distilled water); Group II, Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> NPs (received 30 mg/kg bw Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> NPs); Group III, melatonin and Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> NPs (received 30 mg/kg bw Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> NPs + 10 mg/kg bw melatonin); Group IV, melatonin (received 10 mg/kg bw melatonin). All treatments were administered daily for 28 days by gastric gavage. After that, all rats were sacrificed, then, the samples from different spinal cords were subjected to histopathological, biochemical, and immunohistochemical analyses. Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> NPs markedly elevated malondialdehyde and 8‐hydroxydeoxyguanosine while inhibiting superoxide dismutase and catalase. Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> NPs also induced histological alterations in both gray and white matter manifested by neuronal degeneration, vacuolation, axonal degeneration, ballooning, and fusion of myelin sheaths. Furthermore, immunohistochemical results displayed a strong positive expression of caspase‐3. Conversely, melatonin significantly mitigated the effects of Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> NPs by increasing the activities of antioxidant enzymes and inhibiting malondialdehyde and 8‐hydroxydeoxyguanosine. Moreover, melatonin alleviated most histological alterations induced by Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> NPs and reduced caspase‐3 immunoreactivity. Collectively, melatonin could protect the spinal cord and mitigate Al<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> NPs‐induced neurotoxicity.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"14 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142867282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"αCypermethrin-Induced Biochemical and Molecular Cascades Underlying Ovine Ovarian Granulosa Cell Dysfunctions.","authors":"Poonam Kumari Singh, Bogapathi Sampath Kumar, Sumanta Nandi, Paluru Subramniyam Parameswara Gupta, Sukanta Mondal","doi":"10.1002/tox.24459","DOIUrl":"https://doi.org/10.1002/tox.24459","url":null,"abstract":"<p><p>The present study was conducted to evaluate the impact of α-Cypermethrin (αCYP), the second most commonly used pesticide in India, on the ovine ovarian granulosa cells (GCs) viability, growth, apoptosis, and steroidogenesis. GCs collected from abattoir-derived ovine ovaries were cultured for 3/6 days in the presence of various concentrations of αCYP (0, 1, 10, 25, 50, and 100 μM). The results revealed a binary effect on GCs, where metabolic activity and viability rates were significantly (p < 0.05) lower from 25 μM onwards. Estrogen concentration was significantly low from the 1 μM dose, whereas progesterone concentration showed a significant increase (10 μM) in the spent media of cultured GCs. The cytotoxicity in the GCs exposed to αCYP revealed significant changes in LDH, ROS, CUPRAC, and GST activity (all at 25 μM) and MDA (at 10 μM) compared to those observed in the control group. The gene expression profiles of cultured GCs showed a significant up-regulation of CYP11A1, FSHR (all at 1 μM), StAR, BAX, and CASP3 (all at 10 μM), 3βHSD1 (at 25 μM), and significant down-regulation of CYP17A1 and ERS2 (all at 25 μM), CYP19A1 and 17βHSD (all at 1 μM), ESR1 and BCL2 (all at 10 μM) in comparison to those observed in control groups. The results of the present experiment demonstrated that αCYP affected the growth and functional parameters of GCs, the expression of steroid hormone-associated genes, and hormone secretion.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PM_2.5 Induces the Instability of Atherosclerotic Plaques by Activating the Notch Signaling Pathway In Vivo and In Vitro.","authors":"Tianyang Zhao, Yuezhu Zhang, Xu Li, Zhili Ge, Jingjing Shi, Tianyou Wang, Jiaxin Zhang, Xinyu Zhang, Huibin Jiang, Liting Zhou, Lin Ye","doi":"10.1002/tox.24461","DOIUrl":"https://doi.org/10.1002/tox.24461","url":null,"abstract":"<p><p>Fine particulate matter (PM_2.5) can exacerbate the instability of atherosclerotic plaques although the exact chemical process driving atherosclerosis remains unknown. In order to create atherosclerotic models, a high-fat diet and vitamin D3 injections were given to 56 Wistar rats in this investigation. The atherosclerotic rats were split into four groups at random and given different doses of PM_2.5 (0, 1.5, 7.5, and 37.5 mg/kg) for 4 weeks. To investigate the mechanism, foam cells were exposed to PM_2.5 (0, 25, 50, and 100 μg/mL) for 24 h. The results showed that PM_2.5 exposure caused collagen fibers thinner and muscle fibers were disorganized. PM_2.5 exposure significantly affected the expression of MMP2, MMP9, TIMP2, and vimentin in aortas of atherosclerotic rats. Moreover, PM_2.5 exposure increased the expression of the Notch signaling pathways which was correlated with the expression of atherosclerotic plaque stability-related genes. PM_2.5 exposure also increased the apoptosis rate of foam cells. The expression of MMP2, MMP9, and vimentin was increased and TIMP2 was decreased with the increasing PM_2.5 dose in foam cells. The inhibition of the Notch signaling pathway can alleviate the alteration of atherosclerotic plaque stability-related genes. The findings demonstrated that PM_2.5 exposure can cause atherosclerotic plaques to become unstable, aggravating the progression of atherosclerosis, a process in which the Notch signaling pathway is crucial.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Flurochloridone on the Developmental Toxicity in Zebrafish (Danio rerio) Embryo.","authors":"Mingjun Yang, Jingying Hu, Fang Tian, Minjie Xia, Zhijun Zhou, Weihua Li","doi":"10.1002/tox.24460","DOIUrl":"https://doi.org/10.1002/tox.24460","url":null,"abstract":"<p><p>Flurochloridone (FLC) is a selective herbicide that can cause reproductive toxicity in male rats. However, limited information is available regarding the toxicity of FLC in the developmental stages of aquatic organisms. This study aimed to investigate the effects of FLC exposure during embryonic development and elucidate its potential mechanism of action. Zebrafish embryos were exposed to 6.25, 12.5, 25, and 50 μg/mL FLC for 4-144 hpf. The developmental status of embryos was recorded; the indicators of oxidative stress and embryonic apoptosis were determined. We found that FLC exposure caused severe embryonic malformations, such as pericardial edema, spinal curvature, and growth retardation, accompanied by a decreased hatching and survival rate. After exposure until 144 h postfertilization, the median lethal concentration (LC₅₀) of FLC in zebrafish embryos was 36.9 μg/mL. Subsequently, FLC induced the accumulation of reactive oxygen species and malondialdehyde, enhanced the activity of superoxide dismutase, and activated the Keap1-Nrf2 signaling pathway. Further studies confirmed that FLC can induce apoptosis in zebrafish embryos through the activation of caspase. These results suggest that FLC induced developmental toxicity in zebrafish embryos, which provides new evidence regarding FLC toxicity in aquatic organisms and to assess human health risks.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"3-Chloro-1,2-Propanediol Exposure Induces Cardiotoxicity and Behavioural Abnormalities in Zebrafish Embryos.","authors":"Jing Wang, Qiang Yuan, Weitao Hu, Zhijun Ye, Li Zhang, Zhipeng Wang, Jiejun Liu, Ling Huang, Fasheng Liu, Xinjun Liao, Juhua Xiao, Shouhua Zhang, Zigang Cao","doi":"10.1002/tox.24440","DOIUrl":"https://doi.org/10.1002/tox.24440","url":null,"abstract":"<p><p>Numerous contemporary diseases are linked to food contamination. Pathogenic agents might stem from certain food ingredients or result from pollution stemming from food processing or packaging. One such contaminant is 3-Chloro-1,2-propanediol (3-MCPD), it has been previously reported to be produced during the preparation of chemical sauces, as well as during the heating of baked goods. Yet, uncertainty surrounds its potential to induce embryonic developmental toxicity. In this study, zebrafish were employed as the focal point to assess the impact of 3-MCPD on initial embryonic development, heart functionality, and behavior. The research unveiled that exposure of zebrafish embryos to 18, 36, and 54 mM 3-MCPD led to cardiac anomalies, including pericardial edema, reduced heart rate, and elongated SV-BA distance. Additionally, 3-MCPD exposure triggered aberrations in cardiac-related gene expression and an elevation in oxidative stress. Notably, behavioral changes were observed in 3-MCPD-exposed zebrafish embryos, while vascular development appeared unaffected. This study introduces a novel basis for comprehensive exploration of 3-MCPD toxicity.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2024-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to \"Biochemical Study on the Protective Effect of Curcumin on Acetaminophen and Gamma-Irradiation Induced Hepatic Toxicity in Rats\"M. M. T. Eassawy, A. A. M. Salem, and A. F. M. Ismail, \"Biochemical Study on the Protective Effect of Curcumin on Acetaminophen and Gamma-Irradiation Induced Hepatic Toxicity in Rats,\" Environmental Toxicology 36 (2021): 748-763, https://doi.org/10.1002/tox.23077.","authors":"","doi":"10.1002/tox.24458","DOIUrl":"https://doi.org/10.1002/tox.24458","url":null,"abstract":"","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142767374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Esculin, a Coumarin Glucoside Prevents Fluoride-Induced Oxidative Stress and Cardiotoxicity in Zebrafish Larvae.","authors":"Srija Babu, Naveen Surya Velmani, Suryaa Manoharan, Ekambaram Perumal","doi":"10.1002/tox.24445","DOIUrl":"https://doi.org/10.1002/tox.24445","url":null,"abstract":"<p><p>Fluoride (F^-) is a major groundwater contaminant spread across the world. In excess concentrations, F^- can be detrimental to living beings. F^- exposure is linked to cellular redox dyshomeostasis, leading to oxidative stress-mediated pathologies including heart dysfunction. Due to its potent antioxidant properties, various phytochemicals are found to alleviate the symptoms of F^- toxicity. Hence, we explore the protective effect of esculin (Esc), a coumarin glucoside on F^--induced oxidative stress and cardiotoxicity in zebrafish larvae. The experimental groups consisted of NaF (50 ppm) and Esc (100 μM) groups treated alone and in combination with a control group for 6 h. The groups were maintained till 78 hpf after which the level of oxidants (ROS, LPO, and PCC) and antioxidants (GST, GSH, GPx, SOD, and CAT) were assessed. The results revealed that Esc pretreatment restored the depleted antioxidant markers and reduced the levels of oxidant in the Esc+NaF group, exhibiting its antioxidant potential. In addition, analyses of the heartbeat rate and hemoglobin integrity using o-Dianisidine staining were conducted in the control and experimental groups. Esc treatment prevents F^- induced cardiac changes including tachycardia and altered blood flow. Further, the mRNA expression level of antioxidant genes (nrf2, gstp1, hmox1a, prdx1, and nqo1) and cardiac developmental genes (bmp2b, nkx2.5, myh6, and myl7) confirmed that Esc acts as a potent free radical scavenger and antioxidant defense enhancer, protecting zebrafish larvae from NaF-induced oxidative stress and heart dysfunction.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142738769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dextromethorphan Inhibits Osteoblast Differentiation and Bone Regeneration of Rats With Subcritical-Sized Calvarial Defects.","authors":"Yu-Cheng Lai, Zhi-Kang Yao, Tien-Chieh Chang, Chien-Wei Feng, Tsu-Jen Kuo, Yi-Wei Luo, Yen-Hsuan Jean, Hugo Y-H Lin, Zhi-Hong Wen","doi":"10.1002/tox.24447","DOIUrl":"https://doi.org/10.1002/tox.24447","url":null,"abstract":"<p><p>The glutamatergic signaling pathway, which is mediated by N-methyl-D-aspartate (NMDA) receptors, is crucial for osteoblast differentiation and bone function. Dextromethorphan (DXM), a widely used antitussive, is a noncompetitive antagonist of the NMDA receptor. However, the effects of DXM on osteoblast and bone regeneration remain unclear. The present study investigated the effects of DXM on osteogenesis in vitro and in vivo. A MC3T3-E1 preosteoblast cell line was treated with varying concentrations of DXM. Real-time-quantitative polymerase chain reaction (RT-qPCR) and Western-blot analysis were performed to evaluate the expression of osteogenesis-related runt-related transcription factor 2 (RUNX2), osterix (OSX), osteocalcin (OCN), collagen type 1α (Col-1α), and alkaline phosphatase (ALP) after DXM treatment. Zebrafish embryos were incubated with DXM, which had potential to affect the ossification of the vertebrae and skull, and analyzed using calcein staining. Furthermore, we used a rat calvarial defect model to assess the effects of DXM on bone regeneration by using microcomputed tomography. The results indicate that DXM inhibited extracellular mineralization, ALP activity, and the expression of osteogenic markers, namely RUNX2, OSX, OCN, Col-1α, and ALP, in MC3T3-E1 cells. DXM suppressed skeleton ossification in zebrafish and affected bone regeneration in rats with calvarial defects. However, the mineral density of the regenerated bones did not differ significantly between the DXM and control groups. The present study demonstrated that DXM negatively affects the osteogenic function of osteoblasts, leading to impaired skeletal development and bone regeneration. Thus, clinicians should consider the negative effects of DXM on bone regeneration.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142738767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Ameliorative Effect of Betulinic Acid on Oxidative Stress in Mice of Cyclophosphamide-Induced Liver Damage.","authors":"You Huang, Chaoyang Ma, Lijuan Zhu, Li Kong, Chunlin Huang, Wenjiang Yang, Jiayu He, Mingqi Yang, Lin Huang, Liyun Yuan, Jine Yi","doi":"10.1002/tox.24444","DOIUrl":"https://doi.org/10.1002/tox.24444","url":null,"abstract":"<p><p>As a conventional immunosuppressive drug, cyclophosphamide (CYP) exhibits strong hepatotoxicity in clinical applications. Betulinic acid (BA) is a natural triterpenoid that protects against liver damage. However, the underlying mechanism has not yet been elucidated. The purpose of this study was to evaluate the ameliorative effects of BA on CYP-induced hepatotoxicity and further clarify the underlying mechanism. BA pretreatment mitigated CYP-induced liver oxidative damage by alleviating histopathological lesions, reducing reactive oxygen species (ROS) accumulation, and restoring the mRNA expression of antioxidant enzymes (Cu-Sod, Mn-Sod, Cat, and Gsh-Px). BA treatment also suppressed CYP-induced oxidative stress by activating the NRF2 pathway and inhibiting the MAPK signaling pathway. Moreover, BA attenuated CYP-triggered hepatic apoptosis by suppressing excessive mitochondrial fission, boosting mitochondrial fusion, and ameliorating pro-apoptotic protein expression (CASP9 and the ratio of BCL-2/BAX) by blocking the oxidative stress-activated mitochondrial apoptotic pathway. Furthermore, PD98059 (an inhibitor of ERK) and/or BA abated CYP-provoked hepatotoxicity by inhibiting the ERK-MAPK and mitochondrial apoptotic pathways, implying that deactivation of the ERK-mediated mitochondrial apoptotic pathway contributed to the hepatoprotective efficacy of BA against CYP-induced oxidative stress. Therefore, BA could be used as a complementary medicine in patients undergoing CYP treatment owing to its hepatoprotective effects.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142727312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}