Journal of Hazardous Materials, Год журнала: 2024, Номер 485, С. 136931 - 136931
Опубликована: Дек. 18, 2024
Язык: Английский
Journal of Hazardous Materials, Год журнала: 2024, Номер 485, С. 136931 - 136931
Опубликована: Дек. 18, 2024
Язык: Английский
The Science of The Total Environment, Год журнала: 2024, Номер 919, С. 170699 - 170699
Опубликована: Фев. 5, 2024
Язык: Английский
Процитировано
24Aquaculture Reports, Год журнала: 2024, Номер 35, С. 102004 - 102004
Опубликована: Фев. 28, 2024
Nanoplastics (NPs, < 1 μm) have attracted widespread attention due to their potential threats organisms, ecosystem, and public health. However, there is limited research on the effects of NPs cephalopods. Sepia esculenta (Mollusks, Cephalopoda, Sepioidea), an economically major species Sepiidea family in world, well received by consumers for its delicious quality rich nutrition. In present study, S. larvae were treated with polystyrene nanoplastics (PS-NPs) at 50 μg/mL 4 h, then physiological biomarkers (SOD, GSTs MDA) RNA-Seq whole body performed. Research results suggested that PS-NPs exposure had induced oxidative stress larvae. addition, several key genes signaling pathways related obtained based DEGs, GO KEGG enrichment analyses, as PPI construction analysis transcriptome data. This study enriches different organisms provides insights references revealing mechanisms caused molecular level.
Язык: Английский
Процитировано
22Ecotoxicology and Environmental Safety, Год журнала: 2024, Номер 272, С. 116028 - 116028
Опубликована: Фев. 3, 2024
Extensive application of lead (Pb) brought about environmental pollution and toxic reactions organisms. Selenium (Se) has the effect antagonizing Pb poisoning in humans animals. However, it is still unclear how causes brainstem toxicity. In present study, we wanted to investigate whether Se can alleviate toxicity chicken brainstems by reducing apoptosis. One hundred eighty chickens were randomly divided into four groups, namely control group, Se/Pb group. Morphological examination, ultrastructural observation, relative mRNA expressions genes on heat shock proteins (HSPs); selenoproteins; inflammatory cytokines; apoptosis-related factors investigated. The results showed that exposure led tissue damage apoptosis brainstems. Furthermore, an atypical expression HSPs (HSP27, HSP40, HSP60, HSP70, HSP90); selenoprotein family glutathione peroxidase (GPx) 1, GPx2, GPx3, GPx4), thioredoxin reductases (Txnrd) (Txnrd1, Txnrd2, Txnrd3), dio famliy (diodothyronine deiodinases (Dio)1, Dio2, Dio3), as well other selenoproteins (selenoprotein (Sel)T, SelK, SelS, SelH, SelM, SelU, SelI, SelO, Selpb, n1 (Sepn1), Sepp1, Sepx1, Sepw1, 15-kDa (Sep15), selenophosphate synthetases 2 (SPS2)); cytokines (Interleukin (IL-2), IL-4, IL-6, IL-12β, IL-17, Interferon-γ (IFN-γ)); (B-cell lymphoma-2 (Bcl-2), tumor protein 53 (p53), Bcl-2 Associated X (Bax), Cytochrome c (Cyt c), Caspase-3) identified. An reaction induced after Pb. alleviated abnormal HSPs, selenoproteins, cytokines, tissues treated with indicated inflammatory, involved Se-resisted poisoning. Overall, had resistance against poisoning, be act antidote for
Язык: Английский
Процитировано
18International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(1), С. 380 - 380
Опубликована: Янв. 4, 2025
Plant secondary metabolites (PSMs) are a diverse group of bioactive compounds, including flavonoids, polyphenols, saponins, and terpenoids, which have been recognised for their critical role in modulating cellular functions. This review provides comprehensive analysis the effects PSMs on mitochondrial health, with particular emphasis therapeutic potential. Emerging evidence shows that these improve function by reducing oxidative stress, promoting biogenesis, regulating key processes such as apoptosis mitophagy. Mitochondrial dysfunction, hallmark many pathologies, neurodegenerative disorders, cardiovascular diseases, metabolic syndrome, has shown to benefit from protective PSMs. Recent studies show can dynamics, stabilise membranes, enhance bioenergetics, offering significant promise prevention treatment mitochondrial-related diseases. The molecular mechanisms underlying effects, modulation signalling pathways direct interactions proteins, discussed. integration into strategies is highlighted promising avenue improving efficacy while minimising side commonly associated synthetic drugs. also highlights need future research elucidate specific roles individual synergistic within complex plant matrices, may further optimise utility. Overall, this work valuable insights health potential natural agents targeting dysfunction.
Язык: Английский
Процитировано
3Poultry Science, Год журнала: 2025, Номер 104(4), С. 104965 - 104965
Опубликована: Март 1, 2025
Ammonia (NH3) and lipopolysaccharide (LPS), common pollutants in poultry farming environments, pose significant health risks by disrupting cellular processes. Although previous studies have demonstrated the individual effect of NH3 or LPS on human animal health, mechanisms underlying their combined impact chicken heart tissue remain poorly understood. In this study, we established a cardiotoxicity model to investigate effects and/or exposure energy metabolism, autophagy, endoplasmic reticulum (ER) stress, apoptosis cardiomyocytes. Our findings indicated that or/and reduced ATPase activity ATP content, led downregulation HK2, PK, PDHX, SDH, upregulation AMPK, resulting impaired metabolism Additionally, found gga-miR-1599/HK2 axis as key regulator involved LPS-induced impairment. The impairment activated AMPK/mTOR pathway, which subsequently triggered evidenced Beclin, LC3-I, LC3-II. Furthermore, decreased mTOR expression induced ER markers such ATF6, GRP78, IRE1, PERK. turn, increased CHOP expression, downregulated Bcl-2 upregulated Bim, elevated levels Bax, caspase-9, caspase-3, ultimately triggering apoptosis. This study provides valuable insights into co-exposure identifies potential molecular targets for mitigating these adverse effects.
Язык: Английский
Процитировано
1Poultry Science, Год журнала: 2024, Номер 103(6), С. 103674 - 103674
Опубликована: Март 16, 2024
Microplastics biological toxicity, environmental persistence and chemicals have been paid widespread attention. exposed to chicken spleen injury of the specific mechanism is unclear. Thus, we randomly assigned chickens 4 groups: C (normal diet), L-MPs (1 mg/L), M-MPs (10 H-MPs (100 assessed damage after 42 d exposure. Morphologically, boundary between red white pulp was blurred, along with expansion pulp. It further speculated that microplastics induced mitochondrial dynamic homeostasis (Drp1 upgraded, Mfn1, Mfn2, OPA1 reduced), provoked apoptotic pathway (Bcl-2/Bax decreased, cytc, caspase3, caspase9 raised), resulting in redox imbalance lipid peroxide accumulation (MDA increased, CAT, GSH, T-AOC plummeted), stimulated ferroptosis (FTH1, GPX4, SLC7A11 decreased). Here explored impact polystyrene on spleen, as well programmed death (apoptosis ferroptosis) involved, regulative role mitochondria this process. This could be significant importance bridging gap laboratory research microplastics-induced chicken.
Язык: Английский
Процитировано
7Environmental Pollution, Год журнала: 2024, Номер unknown, С. 124923 - 124923
Опубликована: Сен. 1, 2024
Язык: Английский
Процитировано
4Chemico-Biological Interactions, Год журнала: 2025, Номер unknown, С. 111492 - 111492
Опубликована: Март 1, 2025
Язык: Английский
Процитировано
0The Science of The Total Environment, Год журнала: 2023, Номер 912, С. 169036 - 169036
Опубликована: Дек. 5, 2023
Язык: Английский
Процитировано
10Journal of Agricultural and Food Chemistry, Год журнала: 2024, Номер 72(28), С. 15948 - 15958
Опубликована: Июль 5, 2024
Copper (Cu) is a common trace element additive in animal and human foods, excessive intake of Cu has been shown to cause hepatotoxicity, but the underlying mechanism remains unclear. Our previous research found that exposure dramatically upregulated mitochondrial miR-12294-5p expression confirmed its targeted inhibition CISD1 chicken hepatocytes. Thus, we aimed explore potential role mitomiR-12294-5p/CISD1 axis exposure-resulted hepatotoxicity. Here, observed resulted accumulation pathological injury livers. Moreover, caused mitochondrial-dependent ferroptosis hepatocytes, which were prominent on increased Fe2+ lipid peroxidation, inhibited levels CISD1, GPX4, DHODH, IDH2, also enhanced level PTGS2. Notably, identified mitomiR-2954 effectively mitigated Cu-exposure-resulted peroxidation prevented development ferroptosis. However, increasing mitomiR-12294-5p considerably aggravated influence these indicators. Meanwhile, overexpression alleviated Cu-caused ferroptosis, while silent eliminated therapeutic inhibitor. Overall, our findings indicated played critical function hepatotoxicity chickens by regulating
Язык: Английский
Процитировано
3