{"topic_id":"evidence_exotic_hamster_toxicology","category":"evidence","context":"---\ntopic_id: evidence_exotic_hamster_toxicology\ncategory: evidence\ntitle: \"Evidence cluster — Hamster (Mesocricetus auratus) toxicology (peer-reviewed, Europe PMC)\"\nlang: en\nsource: \"Europe PMC (Europe PubMed Central) REST search, first-hand peer-reviewed abstracts, pulled 2026-08-01\"\nsource_file: pdf-raw/evidence/europepmc_hamster_toxicology_2026-08-01.txt\ndate_parsed: 2026-08-01\ntokens_estimated: 5204\nverification:\n  method: substring_match\n  claims: 12\n  passed: 12\n  date: 2026-08-01\nsource_document: \"Peer-reviewed Hamster toxicology literature (Europe PMC, first-hand abstracts)\"\ncitation:\n  authority: \"Europe PMC\"\n  title: \"Evidence cluster — Hamster (Mesocricetus auratus) toxicology (peer-reviewed, Europe PMC)\"\n  url: \"https://www.ebi.ac.uk/europepmc/\"\n  retrieved: \"2026-08-01\"\n  doc_type: \"first-hand abstracts (Europe PMC REST)\"\n  needs_review: false\n---\n\n# Evidence: Hamster (Mesocricetus auratus) toxicology\n\nSource: Europe PMC (Europe PubMed Central) REST search — first-hand peer-reviewed abstract records, pulled 2026-08-01.\nQueries covered toxicology, poisoning, intoxication, heavy metals, mycotoxins and (for relevant taxa) envenomation for Mesocricetus auratus.\nThe cluster returns **12** representative studies with abstracts below. Abstract text is verbatim from source; each study is traceable by PMID.\n\n## Studies\n- **PMID 42525182 (2026, Cardiovascular toxicology)** — The ApoE-Null Golden Hamster: A Novel Model of Atherosclerosis.. Abstract (opening): Atherosclerosis is a chronic, progressive arterial disease characterized by the deposition of lipids on the inner arterial walls, leading to plaque formation and serious cardiovascular events. Traditional mouse models of atherosclerosis require prolonged dietary induction to exhibit arterial lesions due to significant differences in lipid metabolism compared to humans. In contrast, Golden hamsters share a lipid metabolic profile more closely aligned with humans. In this study, we utilized CRISPR/Cas9 to generate ApoE knockout (ApoE<sup>-/-</sup>) hamsters using, which spontaneously developed atherosclerotic lesions in the arterial wall after 8 weeks on a standard chow diet. When fed on a high-cholesterol/high-fat diet, they exhibited even more severe aortic atherosclerosis, fatty liver, and liver fibrosis. Our findings demonstrated that the ApoE<sup>-/-</sup> hamster model is highly valuable tool for translational research, offering significant potential for studying hyperlipidemia and atherosclerosis in a context more relevant to human physiology.\n  Source: https://pubmed.ncbi.nlm.nih.gov/42525182/\n- **PMID 42227179 (2026, Journal of proteome research)** — The Liver S9 Proteome of Rat and Hamster: Global Profiling and Targeted Cytochrome P450 Quantification Reveal Induction-Responsive Remodeling.. Abstract (opening): A comprehensive global proteomic profiling of rat and hamster liver S9 fractions was conducted under basal conditions and following induction with Aroclor 1254 (Aroclor) or phenobarbital/β-naphthoflavone (PBNF). More than 8500 proteins were quantified across conditions. Induction remodeled xenobiotic pathways with conserved increases in CYP1A and CYP2B, larger CYP3A responses in rats under Aroclor, and prominent CYP2F/CYP2G changes in hamsters, alongside a downshift in mitochondrial electron transport and activation of proteostasis networks (heat-shock chaperones). Complementary targeted analysis with stable isotope-labeled standards enabled absolute quantification of 15 cytochrome P450 enzymes, confirming significant inducer-dependent increases across species. This study integrates global proteomic analysis with absolute quantification of CYPs predominantly involved in drug and nitrosamine metabolism for representative enzymes spanning the CYP1A, CYP2A, CYP2C, CYP2D, CYP2E, and CYP3A families in induced and uninduced rat and hamster S9 fractions. The data set and assays serve as a practical reference for DMPK, toxicology, and nitrosamine activation studies and support selection of inducers to tune CYP-mediated oxidative capacity.\n  Source: https://pubmed.ncbi.nlm.nih.gov/42227179/\n- **PMID 42438898 (2026, Journal of cellular and molecular medicine)** — Therapeutic Efficacy of Indole-3-Carbinol Against SARS-CoV-2-Induced Acute Respiratory Distress Syndrome: A Dual Antiviral and Anti-Inflammatory Approach in a Golden Syrian Hamster Model.. Abstract (opening): SARS-CoV-2 has caused a global pandemic, resulting in over two million deaths and creating an urgent need for effective treatments. Severe COVID-19 is frequently complicated by respiratory failure and acute respiratory distress syndrome (ARDS), the primary drivers of mortality. Indole-3-Carbinol (I3C), a natural compound derived from Brassicaceae that acts as an inhibitor of HECT family E3 ubiquitin ligases, exhibits potent anti-SARS-CoV-2 activity and inhibits viral egress. However, its in vivo therapeutic efficacy against SARS-CoV-2-induced lung injury remains unproven. We evaluated the therapeutic efficacy of I3C in reducing the severity of SARS-CoV-2 infection and associated lung lesions using the Syrian golden hamster (Mesocricetus auratus) model, which recapitulates the acute lung injury observed in human COVID-19. Treatment with a non-toxic dose of I3C (2 mg) significantly ameliorated disease across all parameters, reducing weight loss, improving clinical symptom scores and reducing histopathological lung damage observed post-mortem. A significant reduction in pulmonary TNF-α levels accompanied this. These findings indicate that I3C mitigates COVID-19-related morbidity at clinically relevant, non-toxic doses. Given its dual antiviral and anti-inflammatory mechanisms, I3C represents a compelling therapeutic candidate for further clinical investigation.\n  Source: https://pubmed.ncbi.nlm.nih.gov/42438898/\n- **PMID 42406842 (2026, Journal of visualized experiments : JoVE)** — Investigating The Network-Wide Mechanisms of Pallidal Deep Brain Stimulation Using High-Density Microelectrode Arrays.. Abstract (opening): Dystonia is a neurological movement disorder characterized by abnormal muscle control affecting voluntary movements and sustained postures. Although dystonia is associated with basal ganglia dysfunction, increasing evidence suggests that the cerebellum is involved in its pathophysiology. This protocol presents in vivo pallidal deep brain stimulation (DBS) in a dystonic hamster model (dt<sup>sz</sup> hamster) combined with ex vivo high-density microelectrode array (HD-MEA) recordings to investigate cerebellar activity. The protocol includes (1) DBS surgery for electrode and stimulator implantation, (2) acute cerebellar slice preparation, (3) high-resolution electrophysiological recordings, and (4) data analysis. Representative results indicate that 11 days of pallidal DBS restored spike activity toward normal levels in the molecular, Purkinje, and granular layers, consistent with cerebellar network involvement in dystonia. This protocol enables detailed analysis of cerebellar activity and its modulation by DBS, providing a platform to investigate network-level mechanisms underlying neuromodulation therapies.\n  Source: https://pubmed.ncbi.nlm.nih.gov/42406842/\n- **PMID 41949803 (2026, Experimental & applied acarology)** — Transstadial and transovarial perpetuations of Borrelia venezuelensis in Ornithodoros rudis, with demonstration of vector competence.. Abstract (opening): Ticks of the genus Ornithodoros are recognized vectors of relapsing fever group Borrelia, such as Borrelia venezuelensis, whose infection dynamics in its vector, Ornithodoros rudis, remains poorly understood in Brazil. This study aimed to investigate the transstadial perpetuation and transovarial transmission of B. venezuelensis in O. rudis and the vector competence of all parasitic stages of this tick species. Experimental colonies were maintained under controlled laboratory conditions, and ticks were fed on Syrian hamsters (Mesocricetus auratus). Infection in hamsters was monitored using dark field microscopy and real-time PCR. Borrelia venezuelensis was detected across multiple tick life stages, and its presence in larvae derived from infected females confirmed transovarial transmission. Vector competence for B. venezuelensis was demonstrated for larvae, nymphs and adults of O. rudis. Additionally, neurological symptoms and sudden death were observed in some hamsters, possibly associated with toxicosis due to heavy tick infestation. These findings provide the first experimental evidence of transstadial and transovarial maintenance of B. venezuelensis in O. rudis, reinforcing its role as a competent vector and contributing to a better understanding of the eco-epidemiology of relapsing fever in South America.\n  Source: https://pubmed.ncbi.nlm.nih.gov/41949803/\n- **PMID 42228136 (2026, Archives of toxicology)** — The in vitro alkaline comet assay with liver models as a complementary tool for genotoxicity assessment of N-nitrosamines.. Abstract (opening): N-nitrosamine (NA) impurities in pharmaceuticals represent \"cohort of concern\" compounds under ICH M7(R2), due to their mutagenic/carcinogenic potential, involving cytochrome P450 (CYP)-mediated metabolic activation. Increasing interest in mammalian cell-based genotoxicity/mutagenicity assays prompted our assessment of the in vitro alkaline comet assay regarding its predictive power for NAs. Here, precision-cut liver slices (PCLiS), primary human hepatocytes (PHH), primary rat hepatocytes (PRH), and HepG2 cells with rat or hamster S9-mix were investigated as in vitro model systems. Metabolic competence was characterized beforehand. For performance evaluation, a panel of known-mutagenic [N-nitroso-dimethylamine (NDMA), N-nitroso-diethanolamine, N-nitroso-methylaniline, S-N-nitroso-nornicotine, N-methyl-N-nitroso-2-propanamine] and reported non-mutagenic (methyl-t-butylnitrosamine, N-nitrosoproline) was tested, together with Nitrosamine Drug Substance-Related Impurities [N-nitrosodesloratadine, N-nitrosofolic acid, N-nitrosofluoxetine (NFluo)] at a concentration range of 0.005-10 mM. After 2 h (PCLiS, PHH and PRH) or 4 h (HepG2), NDMA concentration-dependently induced DNA strand breaks in all in vitro models. Sensitivity/specificity of the various liver cell models for prediction of carcinogenic NAs were 100%/50% (HepG2 with hamster S9-mix), 50%/100% (PHH, PRH), and 50%/50% (HepG2 with rat S9-mix), respectively. Benchmark dose modeling indicated a higher relative in vitro comet assay response for NFluo compared to NDMA in all cell systems. In conclusion, the in vitro comet assay represents a sensitive and/or specific tool for complementing regulatory in vitro tests in prediction of mutagenic NAs. However, further optimization work is needed, using expanded training sets of compounds and thorough validation of liver cell models, before the in vitro comet assay could be incorporated in the standard battery for genotoxicity testing.\n  Source: https://pubmed.ncbi.nlm.nih.gov/42228136/\n- **PMID 42219787 (2026, Environmental and molecular mutagenesis)** — Computational Analysis of Differentially Expressed Genes in Arsenic-Induced Carcinogenesis and Their Effect on Human Repair Mechanisms.. Abstract (opening): Arsenic poisoning significantly elevates the risk of cancer and other chronic illnesses. The goal of this research is to identify important genes whose expression changes in response to arsenic toxicity, and the molecular pathways affected by arsenic, using computational analysis of arsenic toxicity profiles. This approach will computationally identify and analyze genes whose expression changes in response to arsenic, thereby elucidating the heightened risk of carcinogenesis in arsenic-exposed individuals. This work employed high-throughput arsenic toxicity profiles to computationally identify and analyze expressed genes (DEGs) differentially in Affymetrix microarray datasets from the Gene Expression Omnibus (GEO) database, which were screened using the GEO2R program. A protein-protein interaction (PPI) network was constructed using STRING to elucidate the functional links between these DEGs and DNA repair genes. Interactions between the seven central genes (E2F1, EXO1, EZH2, FEN1, HIST1H3A, POLA1, and TIMELESS) and the repair genes PARP1, NBN, PMS1, MSH3, XRCC5, XRCC6, MGMT, and MLH1 were discovered. We employed the DAVID and Enrichr-KG platforms to investigate the functions of these genes and their associations with cellular and molecular processes in greater detail. Two hundred eighty-one non-synonymous single-nucleotide polymorphisms (nsSNPs) in the 07 genes linked to arsenic toxicity were found using the COSMIC database. Based on our analysis, mutations in E2F1, EXO1, EZH2, FEN1, HIST1H3A, POLA1, and TIMELESS can hinder DNA repair mechanisms, ultimately leading to cancer. Our computational analysis demonstrated that these non-synonymous SNPs can affect gene function, potentially altering protein stability and activity. Furthermore, according to Metal-Protein docking and protein-protein docking, these genes and their mutations appear to affect interactions with repair proteins substantially. Specific dietary consumption may lessen the detrimental effects of arsenic poisoning on protein function. We hypothesized that the mutations might be reversed by attaching particular molecules to these mutants. The protective effects of six curcumin compounds were examined using molecular docking with AutoDock 4.2.6 to assess protein dynamics and binding interactions. Optimal complexes were selected for dynamics simulation using GROMACS, and potential strategies for long-term cancer prevention related to arsenic exposure were identified.\n  Source: https://pubmed.ncbi.nlm.nih.gov/42219787/\n- **PMID 41932361 (2026, Journal of proteomics)** — Proteomic analysis of ammonia-induced stress in Chinese hamster ovary (CHO) cell cultures.. Abstract (opening): Ammonia (NH₃) and its ionic form ammonium (NH₄<sup>+</sup>) are both metabolic waste products and essential nitrogen sources within Chinese hamster ovary (CHO) cell cultures. Although necessary for amino acid synthesis, excessive accumulation in the extracellular environment can exert stress, reducing cell proliferation and impairing the efficiency of recombinant protein production. Proper endoplasmic reticulum (ER) function is critical for CHO cells as biotherapeutic producers. Previous work has linked elevated ammonia concentrations to reduced productivity via altered N-glycosylation pathways, but its broader effects on ER biology remain unclear. In this study, we applied high-resolution mass spectrometry to perform a comprehensive analysis of changes in the ER proteome in CHO cells exposed to two ammonia concentrations, 10 mM and 30 mM, 48 and 120 h after supplementation. Both conditions suppressed cell growth and reduced product titre; however, the 10 mM supplementation resulted in a minor increase in specific cell productivity. Gene Ontology analysis revealed that ammonia strongly affected the tricarboxylic acid cycle, as well as key metabolic, catabolic and biogenetic processes. Several ER membrane proteins, including HMGCR and PREB, were consistently downregulated. In extended cultures, transmembrane proteins linked to Golgi-transport were upregulated, while vesicle transport associated proteins were downregulated, indicating altered intracellular trafficking. SIGNIFICANCE: This study provides a novel perspective on CHO cell biology under environmental stress by investigating the impact of ammonia accumulation in culture. Despite its presence in CHO culture, ammonia has been relatively under-investigated, compared to other culture conditions. Using high-throughput mass spectrometry for comprehensive proteomic profiling, we characterise the cellular response to ammonia build-up with a level of depth not previously applied to the study of this biological stressor. By specifically analysing proteins localised to the ER, we identify candidate pathways and molecular mechanisms that contribute to reduced CHO cell growth and productivity, offering insights directly relevant to industrial bioprocessing conditions. The link between ammonia concentration and a decrease in productivity has previously been linked to genes involved in N-glycosylation of the recombinant biotherapeutic, but the full extent of ammonia stress on ER function has not yet been investigated. These methods were applied to two IgG producing CHO cell lines to allow for comparison of cell line specific stress adaptations, as well as comparing the short- and long-term effects of excess ammonia.\n  Source: https://pubmed.ncbi.nlm.nih.gov/41932361/\n- **PMID 42312592 (2026, Journal of biochemical and molecular toxicology)** — Hesperidin Methyl Chalcone Inhibits Hallmarks of Cancer by Targeting the AKT, PI3K/GSK-3β/β-Catenin/STAT3 Signaling Axis in Oral Squamous Cell Carcinoma Models.. Abstract (opening): Oral squamous cell carcinoma (OSCC) is the most prevalent and drug-resistant cancer. We studied the chemopreventive effects of Hesperidin Methyl Chalcone (HMC) on DMBA-induced hamster buccal pouch carcinogenesis (HBPCs). Male golden Syrian hamsters developed oral tumors on their left buccal pouches after being treated with 0.5% DMBA topically three times a week for 10 weeks. These findings suggest that well-developed squamous cell carcinomas were highly differentiated, exhibiting hyperplasia and dysplasia. Hamsters with DMBA-painted buccal mucosal tissue were treated with HMC, which greatly improved the biochemical and histological changes. In addition, in silico analysis was performed to anticipate possible protein targets for this medication, including Akt, Pi3k, GSk-3β, β-catenin, and STAT3. HMC has a high binding affinity to the above proteins. The current study reveals that HMC has strong chemopreventive properties and protects the Akt, Pi3k, GSk-3β, β-catenin, and STAT3 proteins, which were considerably changed during DMBA-induced oral carcinogenesis.\n  Source: https://pubmed.ncbi.nlm.nih.gov/42312592/\n- **PMID 41640952 (2026, World journal of hepatology)** — Enhanced surgical tolerance of schistosomiasis-induced fibrotic liver following treatment with &lt;i&gt;Ziziphus&lt;/i&gt; plant extract.. Abstract (opening): <h4>Background</h4><i>Ziziphus spina-christi</i> leaf extract (ZSCLE) can be used to treat hepatic schistosomiasis. However, its role as an anti-inflammatory and anti-proliferative agent remains unexplored.<h4>Aim</h4>To assess the therapeutic potential of ZSCLEs in hamsters infected with <i>Schisto</i> <i>som mansoni</i> (<i>S. mansoni</i>) undergoing 50% liver resection (LR).<h4>Methods</h4>Fifty hamsters were divided into five groups (10 hamsters each), with group I serving as the control; group II received ZSCLE treatment only; group III was infected with <i>S. mansoni</i> but was untreated; group IV was infected with <i>S. mansoni</i> and received ZSCLE treatment; group V was infected with <i>S. mansoni</i> and underwent ZSCLE treatment and 50% LR. Each group was analyzed using DNA flow cytometry, and oxidative stress (nitric oxide levels), inflammatory markers (tumor necrosis factor-α and interferon-γ), and liver biomarkers were assessed. Histopathological examination was conducted for all groups.<h4>Results</h4>Compared with the infected untreated group, the ZSCLE-treated group showed a significant 70.2% reduction in hepatic tissue egg load (3459.5 ± 191.3 <i>vs</i> 1032 ± 25.1, <i>P</i> < 0.001), and the ZSCLE-treated group that underwent surgical resection showed a 71.8% decrease (2021.7 ± 190.2 <i>vs</i> 7193.3 ± 103.4, <i>P</i> < 0.001). Alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and bilirubin levels were higher in group III than in group I, group IV, and group V (<i>P</i> < 0.0001). The liver regeneration rate (%) was significantly higher in group IV and group V than in group III (median values: 45.18%, 47.93% <i>vs</i> 28.31%). Pathological examination revealed fewer granulomas in group V.<h4>Conclusion</h4>ZSCLE-LR is a potent agent against schistosomiasis-induced hepatic damage, exhibiting a significant role in promoting hepatic regeneration. Further molecular-level studies are warranted to investigate the phytochemical properties of ZSCLE and its potential applications in managing schistosomiasis-induced hepatic fibrosis.\n  Source: https://pubmed.ncbi.nlm.nih.gov/41640952/\n- **PMID 41825794 (2026, Biotechnology advances)** — Amino acid metabolism, demand and supply in Chinese Hamster ovary cell culture - A comprehensive literature review.. Abstract (opening): Chinese hamster ovary (CHO) cells serve as the predominant host for the production of recombinant protein biopharmaceuticals. Maintaining an optimal culture environment is critical to achieving high productivity, ensuring protein quality, and minimising production costs. Amino acids are a key component of cell culture media which are essential for promoting cell growth and protein expression. Amino acids are the fundamental building blocks of proteins and serve critical roles in cellular energy generation and biosynthesis. The demand for amino acids varies throughout batch or fed-batch culture, which necessitates careful media and process design to ensure adequate supplies. However, if oversupplied, certain amino acids and associated byproducts can negatively impact cell growth and protein production. This review consolidates our understanding of the complex role of amino acid metabolism in CHO cells in the context of industrial production systems and growth medium formulations. It identifies and discusses key considerations in the demand and supply of amino acids, including fed-batch dynamics, amino acid toxicity, solubility and stability, medium osmolality, amino acid transporters and the relative availability of different amino acids. Based on the synthesis of current knowledge, emerging strategies to balance amino acid supply with demand are discussed, and research priorities identified to advance future efforts to optimise CHO cell culture process and media formulation.\n  Source: https://pubmed.ncbi.nlm.nih.gov/41825794/\n- **PMID 41604429 (2026, PLoS pathogens)** — Membrane-anchored PrPSc is the trigger for prion synaptotoxicity.. Abstract (opening): The mechanism by which prions composed of PrPSc cause the neuropathological aberrations characteristic of prion diseases remains elusive. Previous studies have defined a synaptotoxic signaling pathway in which extracellular PrPSc stimulates NMDA receptor-mediated Ca2+ influx, activation of p38 MAPK, and collapse of the actin cytoskeleton in dendritic spines, resulting in functional decrements in synaptic transmission. However, these studies did not determine whether synaptotoxic signaling is directly linked to conversion of cell-surface PrPC to PrPSc, or whether it can be initiated by extracellular PrPSc independently of PrP conversion. To address this question, we employed two different experimental strategies, both of which interfere with PrPC-PrPSc conversion: (1) neuronal expression of PrPC mutants that are locked in the PrPC conformation (G126V and V208M); and (2) application of extracellular PrPSc from a species (mouse or hamster) that is unable to convert neuronal PrPC of the other species. We first confirmed that both of these strategies resulted in impaired PrPC-PrPSc conversion in cultured N2a and CAD5 cell lines. To assay synaptotoxicity, we then used lentiviral transduction to express the PrPC variants in primary cultures of hippocampal neurons from PrP-null mice, and quantitated dendritic spine density after exposure to purified prions. Expression of G126V PrP completely prevented spine retraction in response to three different murine prion strains (RML, 22L, and ME7), while the effect of V208M PrP was strain-dependent, consistent with partial stabilization of PrP structure by this mutation. Expression of hamster PrPC or mouse PrPC greatly attenuated spine retraction in response to murine 22L and hamster 263K prions, respectively. These findings support a model in which newly formed PrPSc at the neuronal surface is required to initiate prion-mediated synaptotoxic signaling. This work also suggests use of the G126V mutation as part of a therapeutic strategy to reduce PrPSc conversion in prion diseases.\n  Source: https://pubmed.ncbi.nlm.nih.gov/41604429/\n\nSource text: `pdf-raw/evidence/europepmc_hamster_toxicology_2026-08-01.txt` (Europe PMC first-hand abstracts, pulled 2026-08-01).\n","sources":["Europe PMC — Evidence cluster — Hamster (Mesocricetus auratus) toxicology (peer-reviewed, Europe PMC) (retrieved 2026-08-01)"],"source":{"authority":"Europe PMC","title":"Evidence cluster — Hamster (Mesocricetus auratus) toxicology (peer-reviewed, Europe PMC)","url":"https://pubmed.ncbi.nlm.nih.gov/42525182/","retrieved":"2026-08-01","ref":"PMID 42525182","doc_type":"official PDF","source_document":"Peer-reviewed Hamster toxicology literature (Europe PMC, first-hand abstracts)","verification_file":"pdf-raw/evidence/europepmc_hamster_toxicology_2026-08-01.txt"},"source_document":"Peer-reviewed Hamster toxicology literature (Europe PMC, first-hand abstracts)","source_file":"pdf-raw/evidence/europepmc_hamster_toxicology_2026-08-01.txt","tokens_estimated":600,"generated_at":null,"tip":"Use /api/v1/topics to discover more topics. /api/v1/nutrient for precise single-point queries. /api/v1/cross_compare for 2-3 standard comparisons."}