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  Subjects -> PHARMACY AND PHARMACOLOGY (Total: 575 journals)
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Human & Experimental Toxicology
Journal Prestige (SJR): 0.559
Citation Impact (citeScore): 2
Number of Followers: 6  
 
  Hybrid Journal Hybrid journal (It can contain Open Access articles)
ISSN (Print) 0960-3271 - ISSN (Online) 1477-0903
Published by Sage Publications Homepage  [1176 journals]
  • Effects of doxorubicin on autophagy in fibroblasts

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      Authors: Anna Shuey, Conner Patricelli, Julia T Oxford, Xinzhu Pu
      Abstract: Human & Experimental Toxicology, Volume 43, Issue , January-December 2024.
      Objectives: Doxorubicin (DOX) is a highly effective chemotherapeutic used to treat many adult and pediatric cancers, such as solid tumors, leukemia, lymphomas and breast cancer. It can also cause injuries to multiple organs, including the heart, liver, and brain or kidney, although cardiotoxicity is the most prominent side effect of DOX. In this study, we examined the potential effects of DOX on autophagy activity in two different mouse fibroblasts.Methods: Mouse embryonic fibroblasts (NIH3T3) and mouse primary cardiac fibroblasts (CFs) were treated with DOX to assess changes in the expression of two commonly used autophagy protein markers, LC3II and p62. We also examined the effects of DOX the on expression of key genes that encode components of the molecular machinery and regulators modulating autophagy in response to both extracellular and intracellular signals.Results: We observed that LC3II levels increased and p62 levels decreased following the DOX treatment in NIH3T3 cells. However, similar effects were not observed in primary cardiac fibroblasts. In addition, DOX treatment induced the upregulation of a significant number of genes involved in autophagy in NIH3T3 cells, but not in primary cardiac fibroblasts.Conclusions: Taken together, these results indicate that DOX upregulates autophagy in fibroblasts in a cell-specific manner.
      Citation: Human & Experimental Toxicology
      PubDate: 2024-02-07T06:40:16Z
      DOI: 10.1177/09603271241231947
      Issue No: Vol. 43 (2024)
       
  • Widely targeted quantitative lipidomics reveal lipid remodeling in adipose
           tissue after long term of the combined exposure to bisphenol A and
           fructose

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      Authors: Yonghong Tang, Guifang Ou, Ouyan Rang, Xu Liu, Xiaocheng Liu, Xinru Qin, Guojuan Li, Qing Yang, Mu Wang
      Abstract: Human & Experimental Toxicology, Volume 43, Issue , January-December 2024.
      Adipose tissue is the main organ that stores lipids and it plays important roles in metabolic balance in the body. We recently reported in Human and Experimental Toxicology that the combined exposure to BPA and fructose may interfere with energy metabolism of adipose tissue. However, it is still unclear whether the combined exposure to BPA and fructose has the possibility to induce lipid remodeling in adipose tissue. In the present study, we performed a widely targeted quantitative lipidomic analysis of the adipose tissue of rats after 6 months of BPA and fructose combined exposure. We totally determined 734 lipid molecules in the adipose tissue of rats. Principal component analysis (PCA) showed the group of the combined exposure to higher-dose (25 μg/kg every other day) BPA and fructose can be distinguished from the groups of control, higher-dose BPA exposure and fructose exposure clearly. Partial least squares-discriminant analysis (PLS-DA) and univariate statistical analysis displayed lipids of PC(18:0_ 20:3), TG(8:0_14:0_16:0), TG(12:0_14:0_16:1), TG(10:0_16:0_16:1), TG(12:0_ 14:0_18:1), TG(14:0_ 16:0_16:1), TG(14:0_14:1_16:1), TG(8:0_ 16:1_16:2), TG(14:1_16:1_ 16:1), TG(16:1_18:1_18:1), TG(16:0_16:1_20:4) and TG(15:0_18:1_ 24:1) may contributed the most to the discrimination. These findings indicated that combined exposure to BPA and fructose has the potential to cause lipid remodeling in adipose tissue.
      Citation: Human & Experimental Toxicology
      PubDate: 2024-02-06T11:26:17Z
      DOI: 10.1177/09603271241232609
      Issue No: Vol. 43 (2024)
       
  • Estimated mercury vapor exposure from amalgams among American pregnant
           women

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      Authors: David A Geier, Mark R Geier
      Abstract: Human & Experimental Toxicology, Volume 43, Issue , January-December 2024.
      This study examined the impact of mercury (Hg) vapor exposure from amalgams among all American pregnant women. Amalgam-Hg vapor exposure among 1,665,890 weighted-pregnant women (n = 37) was examined in the 2015-2020 National Health and Nutrition Examination Survey (NHANES). Correlation coefficients between amalgam surfaces and daily micrograms (µg) of urinary Hg excretion and daily µg of Hg vapor exposure from amalgams per kilogram (Kg) bodyweight were calculated. Daily Hg vapor exposure from amalgams was compared to Hg vapor safety limits. About 600,000 pregnant women (∼36%) had at least one amalgam surface. Median daily urinary Hg excretion was ∼2.5-fold higher among pregnant women with amalgams as compared to pregnant women without amalgams. A significant correlation was observed between the number of amalgam surfaces and daily urinary Hg excretion. Among pregnant women with amalgams, it was estimated that the median daily Hg vapor dose from amalgams was 7.66 µg of Hg and 0.073 µg of Hg/Kg bodyweight. Among all pregnant women, ∼28% received daily Hg vapor doses from amalgams above the least restrictive United States (US) Environmental Protection Agency (EPA) safety limit and ∼36% received above the most restrictive California (CA) EPA safety limit. Given the potential for fetal toxicological effects from prenatal Hg vapor exposure, special emphasis needs to be placed on reducing/eliminating amalgams in pregnancy/women of reproductive age and future studies should evaluate adverse pregnancy outcomes.
      Citation: Human & Experimental Toxicology
      PubDate: 2024-02-06T03:50:50Z
      DOI: 10.1177/09603271241231945
      Issue No: Vol. 43 (2024)
       
  • Ginsenoside Rg5 induces NSCLC cell apoptosis and autophagy through
           PI3K/Akt/mTOR signaling pathway

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      Authors: Caidie Zhang, Yan Jin
      Abstract: Human & Experimental Toxicology, Volume 43, Issue , January-December 2024.
      ObjectiveGinsenoside Rg5 (Rg5) is a minor ginsenoside of ginseng and has a strong anti-tumor potential. This study focused on deciphering the function of Rg5 in non-small cell lung cancer (NSCLC) and investigating its related mechanism.MethodsAfter treating human NSCLC cell lines (H1650 and A549) and bronchial epithelial cells (BEAS-2B) with increasing concentration of Rg5, cell viability was examined using methyl thiazolyl tetrazolium (MTT) assay. NSCLC cell proliferation and apoptosis were evaluated by colony formation assay and flow cytometry, respectively. The levels of proteins associated with cell cycle progression, cell apoptosis, and autophagy as well as the key markers in the PI3K/Akt/mTOR pathway were measured using western blot. A xenograft nude mouse model was established to explore the function of Rg5 in vivo.ResultsNSCLC cell viability was dose- and time-dependently suppressed after Rg5 treatment. Rg5 restrained NSCLC cell proliferation by inducing G2/M phase arrest via regulation of cell cycle-related genes including p21, cyclin B1, and Cdc2. Additionally, Rg5 promoted caspase-dependent apoptosis in NSCLC cells by regulating the intrinsic mitochondrial signaling pathway. Rg5 induced autophagy via the regulation of autophagy-related proteins. The in vivo experiments revealed the inhibitory impact of Rg5 on xenograft growth. Rg5 also inactivated the PI3K/Akt/mTOR signaling pathway in NSCLC cells and mouse tumors.ConclusionRg5 induced autophagy and caspase-dependent apoptosis in NSCLC cells by inhibiting the PI3K/Akt/mTOR signaling pathway, suggesting that Rg5 might become a promising and novel anti-tumor agent for the clinical treatment of NSCLC patients.
      Citation: Human & Experimental Toxicology
      PubDate: 2024-01-30T02:50:28Z
      DOI: 10.1177/09603271241229140
      Issue No: Vol. 43 (2024)
       
  • Liver and ovarian toxicities boosted by bisphenol and gamma radiation in
           female albino rats

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      Authors: Asmaa A Hassan, Sherein S Abdelgayed, Somaya Z Mansour
      Abstract: Human & Experimental Toxicology, Volume 43, Issue , January-December 2024.
      Bisphenol A (BPA), a carbon-based synthetic polymer compound, was newly classified as an environmental toxicant and an endocrine-disrupting chemical leading to abnormalities in cell proliferation, apoptosis, or migration that contributes to cancer development and progression. This study aims to evaluate the effect of the elevation of γ- radiation dose and BPA on the liver and ovaries of female rats. In this study, eighty female albino rats (130–150 g) were used in this work. Rats in this experiment received BPA in ethanol (50 mg/kg b. wt.) for 30 days, day after day, and in the irradiated groups, animals were administered BPA and then exposed to γ- radiation in doses (2, 4, and 6 Gy) one shot dose. Several members of the cytochrome family were examined. Exposure to γ-radiation and BPA showed an increase in cytochrome P450 and b5 fold change. Further, BPA and γ-radiation activate α and β estrogen receptors and also downregulate aromatase (CYT19) fold change. The current results also revealed that BPA and/or γ-radiation regulate the protein expression of the PI3K/Akt signaling pathway. The steroidogenic acute regulatory protein (StAR) appeared to be targeted by BPA and γ-radiation and its relative expression was elevated significantly by raising the γ-radiation dose. In conclusion, exposure to BPA, an endocrine-disrupting chemical, leads to marked toxicity. Additionally, toxicity is heightened by increasing the γ-radiation dose, either alone or in combination with BPA.
      Citation: Human & Experimental Toxicology
      PubDate: 2024-01-24T07:23:16Z
      DOI: 10.1177/09603271231219264
      Issue No: Vol. 43 (2024)
       
  • Evaluation of antioxidant properties and cytotoxicity of brown algae
           (nizamuddinia zanardinii) in uterine (hela) and pancreatic cancer cell
           lines (paca-2)

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      Authors: Milad Amerifar, Hesamoddin Arabnozari, Mohammad Shokrzadeh, Emran Habibi
      Abstract: Human & Experimental Toxicology, Volume 43, Issue , January-December 2024.
      IntroductionPancreatic cancer and cervical cancer are among the most common cancers. Brown algae have anti-inflammatory, anti-cancer, anti-fungal, antioxidant, and immune-boosting properties. This study investigated the antioxidant properties and the effect of brown algae extract on pancreatic and uterine cancer cells.Materials and methodsIn this study, Cervical (Hela) and pancreas (Paca-2) cancer cell lines were examined. The algae materials were extracted by sequential maceration method and amount of fucoxanthin content in the sample was determined by using High Performance Liquid Chromatography (HPLC) system. The cytotoxic effect of different concentrations of brown algae was measured by the MTT assay. All statistical calculations for comparing IC50 were analyzed using Graph Pad Prism software.Resultsthe algal sample contained an average of 102.52 ± 0.12 μg of fucoxanthin per 100 g. IC50 for 2, 2-diphenyl-1-picrylhydrazyl (DPPH) and hydrogen peroxide free radical scavenging activity for methanolic extract was 2.02 and 11.98 ± 0.13 respectively. Brown algae in all fractions inhibited cell growth and survival. In Hela cell lines, the methanolic extract was the most effective inhibitor, while in Paca cell lines, hexane and methanolic extracts were particularly potent. The methanolic extract was more toxic than other fractions on Hela and Paca cell lines.ConclusionThis study highlights brown algae extracts strong anticancer effects on uterine and pancreatic cancer cells, suggesting its potential as a natural anticancer drug. Different fractions of the extract showed superior apoptotic and cytotoxic effects, with higher concentrations leading to increased apoptotic effects and reduced survival rates of cancer cells.
      Citation: Human & Experimental Toxicology
      PubDate: 2024-01-19T02:09:28Z
      DOI: 10.1177/09603271241227228
      Issue No: Vol. 43 (2024)
       
  • The effect of melatonin on capecitabine-induced hepatic and renal toxicity
           in rats

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      Authors: Ali Tavakoli Pirzaman, Razieh Mansoori, Seyed Mohammad Hosseini, Ali Abolhosseini, Sahar Khosravi, Ali Akbar Moghadamnia, Sohrab Kazemi
      Abstract: Human & Experimental Toxicology, Volume 43, Issue , January-December 2024.
      BackgroundCapecitabine (CAPE), an antimetabolite chemotherapy, can induce hepatic and renal toxicity. Melatonin (MEL), a neurohormone, possesses antioxidant, anti-apoptotic and anti-inflammatory effects. This study investigated the impact of MEL on capecitabine-induced hepatic and renal toxicity.Methods and materialsTwenty-five male Wistar rats were categorized into five groups for the study. The groups included a control group, MEL10 group (rats receiving daily intraperitoneal injections of 5 mg/kg MEL), CAPE 500 group (rats receiving weekly intraperitoneal injections of 500 mg/kg CAPE), CAPE + MEL five group, and CAPE + MEL 10 group. All groups were treated for a duration of 6 weeks. Various hematological, serological, biochemical, and histopathological assessments were conducted to evaluate the objective of the study.ResultsThe administration of CAPE led to significant liver and kidney toxicity, as evidenced by elevated levels of malondialdehyde (MDA), myeloperoxidase (MPO), nitric oxide (NO), as well as serological markers including AST, ALT, ALP, BUN, and creatinine. CAPE exposure also resulted in a reduction in total antioxidant capacity (TAC) and glutathione peroxidase (GPx) levels. Histological examination revealed hyperemia in both liver and kidney tissues exposed to CAPE. However, treatment with MEL demonstrated positive effects. MEL administration alleviated oxidative stress, reduced levels of liver enzymes, BUN, and creatinine, and ameliorated histopathological degenerations. MEL also increased GPx and TAC levels. Moreover, MEL treatment aided in restoring the body weight that was lost due to CAPE exposure.ConclusionOur findings indicated that the administration of MEL in rats significantly enhanced the hepatic and renal toxicity induced by CAPE.
      Citation: Human & Experimental Toxicology
      PubDate: 2024-01-05T08:52:23Z
      DOI: 10.1177/09603271231223506
      Issue No: Vol. 43 (2024)
       
  • Evaluation of Cd-induced cytotoxicity in primary human keratinocytes

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      Authors: Daniil Romashin, Viktoriia Arzumanian, Ekaterina Poverennaya, Alexandra Varshaver, Nataliya Luzgina, Alexander Rusanov
      Abstract: Human & Experimental Toxicology, Volume 43, Issue , January-December 2024.
      An increasing number of studies have investigated the effects of Cd on human health. Cd-induced dermatotoxicity is an important field of research, but numerous studies have focused on the effects of Cd on the human skin. Moreover, most studies have been performed using HaCaT cells but not primary keratinocytes. In this study, we provide the results describing the cytotoxic effects of Cd exposure on primary human epidermal keratinocytes obtained from different donors. The subtoxic concentration of cadmium chloride was determined via MTT assay, and transcriptomic analysis of the cells exposed to this concentration (25 µM) was performed. As in HaCaT cells, Cd exposure resulted in increased ROS levels, cell cycle arrest, and induction of apoptosis. In addition, we report that exposure to Cd affects zinc and copper homeostasis, induces metallothionein expression, and activates various signaling pathways, including Nrf2, NF-kB, TRAIL, and PI3K. Cd induces the secretion of various cytokines (IL-1, IL-6, IL-10, and PGE2) and upregulates the expression of several cytokeratins, such as KRT6B, KRT6C, KRT16, and KRT17. The results provide a better understanding of the mechanisms of cadmium-induced cytotoxicity and its effect on human epidermal skin cells.
      Citation: Human & Experimental Toxicology
      PubDate: 2024-01-04T09:28:03Z
      DOI: 10.1177/09603271231224458
      Issue No: Vol. 43 (2024)
       
  • Gpnmb silencing protects against hyperoxia-induced acute lung injury by
           inhibition of mitochondrial-mediated apoptosis

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      Authors: Xiaoqin Wang, Song Qin, Yingcong Ren, Banghai Feng, Junya Liu, Kun Yu, Hong Yu, Zhenliang Liao, Hong Mei, Mei Tan
      Abstract: Human & Experimental Toxicology, Volume 43, Issue , January-December 2024.
      Background: Hyperoxia-induced acute lung injury (HALI) is a complication to ventilation in patients with respiratory failure, which can lead to acute inflammatory lung injury and chronic lung disease. The aim of this study was to integrate bioinformatics analysis to identify key genes associated with HALI and validate their role in H2O2-induced cell injury model.Methods: Integrated bioinformatics analysis was performed to screen vital genes involved in hyperoxia-induced lung injury (HLI). CCK-8 and flow cytometry assays were performed to assess cell viability and apoptosis. Western blotting was performed to assess protein expression.Results: In this study, glycoprotein non-metastatic melanoma protein B (Gpnmb) was identified as a key gene in HLI by integrated bioinformatics analysis of 4 Gene Expression Omnibus (GEO) datasets (GSE97804, GSE51039, GSE76301 and GSE87350). Knockdown of Gpnmb increased cell viability and decreased apoptosis in H2O2-treated MLE-12 cells, suggesting that Gpnmb was a proapoptotic gene during HALI. Western blotting results showed that knockdown of Gpnmb reduced the expression of Bcl-2 associated X (BAX) and cleaved-caspase 3, and increased the expression of Bcl-2 in H2O2 treated MLE-12 cells. Furthermore, Gpnmb knockdown could significantly reduce reactive oxygen species (ROS) generation and improve the mitochondrial membrane potential.Conclusion: The present study showed that knockdown of Gpnmb may protect against HLI by repressing mitochondrial-mediated apoptosis.
      Citation: Human & Experimental Toxicology
      PubDate: 2024-01-03T02:37:11Z
      DOI: 10.1177/09603271231222873
      Issue No: Vol. 43 (2024)
       
  • Potential induction of hyperkeratosis in rats’ cervi by gentamicin via
           induction of oxidative stress, inflammation and apoptosis

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      Authors: Walaa Yehia Abdelzaher, Mina Ezzat Attya, Mohamed Ahmed Zeen El-Din, Alaa Gamal El Satae, Hatem A Mohamed, Remon R Rofaeil
      Abstract: Human & Experimental Toxicology, Volume 43, Issue , January-December 2024.
      The present study aimed to identify the possible effect of gentamicin (GEN) in Rats’ Cervi. Estradiol Valerate (EV) was used to induce cervical hyperkeratosis. GEN was administered in absence of EV. Serum and cervical GEN concentration were determined. Levels of malondialdehyde (MDA), total nitrites/nitrate (NOx), reduced glutathione (GSH), tumor necrosis factor-α (TNF-α), sirtuin type 1 (Sirt1) and nuclear factor (erythroid-derived 2)-like-2 factors (Nrf2) were measured in cervix tissue. Expression of BAX and Bcl2 were determined. Cervical histopathological examination was done. EV and GEN significantly increased MDA, NOx, TNF-α and BAX/Bcl2 ratio with decrease in GSH, Nrf2 and Sirt1 levels in cervical tissue. Histopathological picture of diffuse and marked hyperkeratosis was detected in EV and GEN groups. In conclusion, GEN-induced cervical hyperkeratosis via induction of oxidative stress, inflammation and apoptosis.
      Citation: Human & Experimental Toxicology
      PubDate: 2024-01-03T01:34:31Z
      DOI: 10.1177/09603271231225744
      Issue No: Vol. 43 (2024)
       
 
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  Subjects -> PHARMACY AND PHARMACOLOGY (Total: 575 journals)
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