Elsevier eBooks, Год журнала: 2024, Номер unknown, С. 359 - 376
Опубликована: Ноя. 29, 2024
Язык: Английский
Elsevier eBooks, Год журнала: 2024, Номер unknown, С. 359 - 376
Опубликована: Ноя. 29, 2024
Язык: Английский
Journal of Agricultural and Food Chemistry, Год журнала: 2024, Номер 72(7), С. 3314 - 3324
Опубликована: Фев. 8, 2024
Fusarium species produce a secondary metabolite known as T-2 toxin, which is the primary and most harmful toxin found in type A trichothecenes. widely food grain-based animal feed endangers health of both humans animals. exposure animals occurs primarily through administration; therefore, first organ that targets gut. In this overview, research progress, toxicity mechanism, detoxification were reviewed, future directions proposed. damages intestinal mucosa destroys structure barrier function; furthermore, disrupts microbiota, causes flora disorders, affects normal metabolic function, kills epidermal cells by inducing oxidative stress, inflammatory responses, apoptosis. The mechanism intestine stress. Currently, selenium plant extracts are mainly used to exert antioxidant effects alleviate enterotoxicity toxin. studies, use genomic techniques find upstream signaling molecules associated with enterotoxin will provide new ideas for prevention toxicity. purpose paper review progress on propose treatment
Язык: Английский
Процитировано
19Mycotoxin Research, Год журнала: 2024, Номер 40(1), С. 85 - 95
Опубликована: Янв. 13, 2024
Язык: Английский
Процитировано
13Journal of Agricultural and Food Chemistry, Год журнала: 2025, Номер unknown
Опубликована: Янв. 27, 2025
T-2 toxin is a highly toxic fungal that threatens humans and animals' health. As major detoxifying metabolic organ, the kidney also target of toxin. This article reviews nephrotoxicity research progress, covering renal structure function damage, mechanisms, detoxification methods to future directions. damages structure, causing dysfunction. The mechanism involves multiple factors including oxidative stress, endoplasmic reticulum mitophagy, inflammatory responses, apoptosis, which are intertwined interdependent. Current strategies mainly involve reducing in feedstuff using antioxidant substances, but both have limits. Future should focus on cells sensitivity toxin, exploring key molecules toxin's nephrotoxicity, injury's impact other organs, better methods. review aims guide underpin toxin-induced prevention treatment.
Язык: Английский
Процитировано
2Deleted Journal, Год журнала: 2025, Номер 2(1)
Опубликована: Фев. 17, 2025
Язык: Английский
Процитировано
2Chemosphere, Год журнала: 2023, Номер 341, С. 140087 - 140087
Опубликована: Сен. 5, 2023
Язык: Английский
Процитировано
13Toxicon, Год журнала: 2024, Номер unknown, С. 107652 - 107652
Опубликована: Фев. 1, 2024
Язык: Английский
Процитировано
5Ecotoxicology and Environmental Safety, Год журнала: 2024, Номер 281, С. 116612 - 116612
Опубликована: Июнь 18, 2024
T-2 toxin is one of trichothecene mycotoxins, which can impair appetite and decrease food intake. However, the specific mechanisms for toxin-induced anorexia are not fully clarified. Multiple research results had shown that gut microbiota have a significant effect on regulation. Hence, this study purposed to explore potential interactions regulate factors in induced by toxin. The divided mice into control group (CG, 0 mg/kg BW toxin) toxin-treated (TG, 1 toxin), oral gavage 4 weeks, construct subacute poisoning mouse model. This data proved was able induce an increased contents gastrointestinal hormones (CCK, GIP, GLP-1 PYY), neurotransmitters (5-HT SP), as well pro-inflammatory cytokines (IL-1β, IL-6 TNF-α) serum mice. disturbed composition microbiota, especially, Faecalibaculum Allobaculum, positively correlated with CCK, GLP-1, 5-HT, IL-1β, TNF-α, played certain role regulating host appetite. In conclusion, changes (especially increase abundance Allobaculum) promote upregulation hormones, neurotransmitters, cytokines, may be mechanism anorexia.
Язык: Английский
Процитировано
5Antioxidants, Год журнала: 2025, Номер 14(5), С. 604 - 604
Опубликована: Май 17, 2025
Cardiovascular diseases (CVDs) remain a leading global health concern, responsible for substantial morbidity and mortality. In recent years, as our understanding of the multifaceted nature CVDs has increased, it become increasingly evident that traditional risk factors alone do not account entirety cardiovascular Environmental toxins, heterogeneous group substances ubiquitous in surroundings, have now entered spotlight offenders development progression CVDs. toxins include heavy metals, air pollutants, pesticides, endocrine-disrupting chemicals, among others. Upon exposure, they can elicit oxidative stress, condition characterized by an imbalance between production reactive oxygen species (ROS) body’s ability to detoxify repair resulting damage. Oxidative stress triggers cascade events, including inflammation, endothelial dysfunction, lipid peroxidation, vascular remodeling, which contribute atherosclerosis, hypertension, other pathologies. This article delves into molecular mechanisms underpinning stress-mediated damage induced environmental emphasizing role specific this process. Further research is necessary understand how individual susceptibility genotype influence impact on CVD.
Язык: Английский
Процитировано
0Molecules, Год журнала: 2024, Номер 29(23), С. 5491 - 5491
Опубликована: Ноя. 21, 2024
T-2 toxin, a highly toxic type A trichothecene, is secondary fungal metabolite produced by various Fusarium species. The consumption of food and feed contaminated with toxin major factor contributing to growth retardation, posing significant risks both human animal health. However, the specific targets mechanisms that mitigate toxin-induced retardation remain unclear. In this study, transcriptomic analysis was employed identify key differentially expressed genes associated alleviation retardation. Peroxiredoxin 4 (PRDX4), gene linked oxidative stress apoptosis, found be one most downregulated in toxin-treated GH3 cells, an vitro model experiments demonstrated significantly increased reactive oxygen species' production, cell cycle arrest while reducing activity antioxidant enzymes (superoxide dismutase glutathione peroxidase) PRDX4 expression cells. Furthermore, silencing exacerbated whereas overexpression effectively mitigated these effects. These findings highlight protective role counteracting suggesting can serve as therapeutic target for treatment
Язык: Английский
Процитировано
2Elsevier eBooks, Год журнала: 2024, Номер unknown, С. 359 - 376
Опубликована: Ноя. 29, 2024
Язык: Английский
Процитировано
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