Foods
·
2024
·Vol. 14
·期 1
·3
·
IF 4.7
Nan Li,Zhigang Yang,Zhiyu Yuan,Zizhu Zhen,Xinna Xie,Danqing Zhu,Gang Lu,Feng Zhao,Bo Qu,Bingli Qi,Yujun Jiang,Qianyu Zhao,Chaoxin Man
This study investigated the variations and alterations in the concentrations of plasmin system components in raw and UHT (ultra-high-temperature) milk under cold stress (WCT ≤ −25 °C), heat stress (THI ≥ 80), and normal (THI < 70 and WCT ≥ −10 °C) circumstances. The findings indicated elevated amounts of plasmin system components in cold-stressed raw milk. While storing UHT milk at 25 °C, the concentrations and activity of plasmin in the milk exhibited an initial increase followed by a decrease, peaking around the 30th day. The maximum plasmin level and activity in cold-stressed milk were 607.86 μg/L and 15.99 U/L, respectively, with the beginning of gelation occurring around day 60. The higher activity of plasmin in cold-stressed milk led to the poorer stability and sensory assessment of the milk. However, heat-stressed milk is not such a problem for UHT milk as cold-stressed milk. The findings indicate shortcomings in the quality of cold-stressed milk and its adverse effects on the stability of UHT milk, underscoring the necessity of preventing cold stress in the herd and refraining from utilizing cold-stressed milk as a raw material for UHT production.
研究领域:
食品科学
·
生物学
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产品关联
DOI
PubMed
高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
·
2024
·
IF 6.2
Dong Li,Wen Cheng,Xiaoping Zhou,Xing Zheng,Jiehui Ren,Ting Meng
Chloro-haloacetonitrile (Cl-HAN), belongs to a group of nitrogenous disinfection by-products (N-DBPs) found in surface water, and are known to pose a major risk to the safety of human drinking water. However, the exact biological toxicity mechanism and the extent of the stress response caused by Cl-HAN remain unclear, resulting in a lack of effective measures to control its presence. Thus, the quantitative toxicological genomics and bioinformatics methods were applied to explore the effects of three chloro-haloacetonitriles (Cl-HANs) on the transcription of fusion genes under varying concentrations of stress in E. coli over 2-hour period. The initial stress response and their toxic mechanism were analyzed. The study also identified the molecular toxicity endpoint, and the core genes that are responsible for the specific toxicity of different Cl-HANs. Cl-HANs exhibited concentration-dependent characteristics of toxic effects, and caused changes in gene expression related oxidative and membrane stress. The stress response results showed that dichloroacetonitrile (dCAN) still caused significant DNA damage under the lowest concentration stress. Chloroacetonitrile (CAN) and trichloroacetonitrile (tCAN) exhibited lower genetic toxicity levels at 513 μg/L and 10.7 μg/L, respectively. The toxic effects of tCAN were widespread. And there was a good correlation between the molecular endpoint (EC-TELI 1.5 ) and the phenotypic endpoint (LD50) with r p =-0.8634 ( P =0.0593). In all concentrations of stress in CAN, dCAN, and tCAN, the number of overexpressed genes shared was 15, 2, and 14, respectively. Furthermore, bioinformatics analysis demonstrated that Cl-HANs affected genes associated with general stress pathways, such as cell biochemistry and physical homeostasis, resulting in changes in biological processes. And for CAN-induced DNA damage, polA played a dominant role, while katG , oxyR , and ahpC were the core genes involved in oxidative stress induced by dCAN and tCAN, respectively. These findings provide valuable data for the toxic effect of Cl-HANs.
研究领域:
环境科学
·
分子生物学
·
毒理学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
·
2025
·
IF 4.9
Fan Mo,Xiaoyi Qin,Xu Zhou,Haoran Jiang,Chong Wang,Yanjun Cui
Heat stress (HS) compromises intestinal barrier integrity and microbiota homeostasis. Trehalose, a nonreducing disaccharide, is well known as a molecular chaperone to prevent protein misfolding under stress. However, whether trehalose supplementation can affect intestinal barrier integrity and microbiota under HS remains unknown. Male C57BL/6 mice (6 week old) were randomly divided into 3 groups (7 mice/group): a normal control group (CON, 23℃), a heat stress group (HS, 42℃) and heat stress + trehalose group (HT, received 2.0% trehalose in drinking water under HS condition). Trehalose supplementation decreased rectal temperature and body weight loss in heat-stressed mice. HS-induced intestinal permeability characterized by increased D-lactate was inhibited by upregulating protein expression of tight junction proteins including occludin and Zo1 in mice administrated by trehalose. Supplementary trehalose significantly ameliorated HS-induced oxidative stress by elevating activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) as well as protein expression of catalase (CAT). Trehalose intervention reversed the up-regulation of endoplasmic reticulum (ER) stress proteins glucose-regulated protein 78 (GRP78), growth arrest and DNA damage-inducible protein 34 (GADD34), phosphorylated eukaryotic initiation factor 2α (p-eif2α), activating transcription factor 4 (ATF4), and C/EBP homologous protein (CHOP) as well as proapoptotic proteins BAX, Cytc, and active-caspase3 in heat-stressed mice. Trehalose supplementation evidently elevated the abundance of beneficial bacteria Lachnospiraceae_NK4A136_group while reducing that of harmful bacteria Bacteroidetes in heat-stressed mice. Taken together, these results revealed that supplementary trehalose could attenuate HS-induced intestinal barrier dysfunction via reducing oxidative stress, reversing ER stress induced apoptosis and gut microbial dysbiosis, suggesting trehalose as a promising dietary additive to counteract the intestinal injury induced by HS in mice.
研究领域:
分子生物学
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营养学
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微生物学
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生理学
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药理学
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产品关联
DOI
PubMed
高影响因子
Frontiers in Pharmacology
·
2024
·
IF 4.4
Shi Yaning,Gao Zhixin,Xu Bing,Mao Junbing,Wang Yue,Liu Zongping,Wang Jicang
Cadmium (Cd) is a highly hazardous toxic substance that can cause serious harm to animals. Previous studies have indicated that cadmium chloride (CdCl2) can damage organs, such as the liver, ovaries, and testicles. Naringenin (Nar) represents a flavonoid with various properties that promote the alleviation of Cd-induced damage. In this experiment, 60 chickens were divided into the control group, 150 mg/kg CdCl2 treatment group, 250 mg/kg Nar treatment group, and 150 mg/kg CdCl2 + 250 mg/kg Nar co-treatment group, which were treated for 8 weeks. Kidney tissues samples were collected to investigate kidney function, including oxidative stress (OS), endoplasmic reticulum (ER) stress, and autophagy activity. Experimental results showed the decreased weight of chickens and increased relative weight of their kidneys after CdCl2 treatment. The increase in NAG, BUN, Cr, and UA activities, as well as the increase in MDA and GSH contents, and the decrease activities of T-AOC, SOD, and CAT in the kidney, manifested renal injury by OS in the chickens. TUNEL staining revealed that CdCl2 induced apoptosis in renal cells. CdCl2 upregulates the mRNA and protein expression levels of GRP78, PERK, eIF2α, ATF4, ATF6, CHOP, and LC3, and inhibited the mRNA and protein expression levels of P62 proteins, which leads to ER stress and autophagy. The CdCl2 + Nar co-treatment group exhibited alleviated CdCl2-induced kidney injury, OS, ER stress, and autophagy. Research has demonstrated that Nar reduces CdCl2-induced kidney injury through alleviation of OS, ER stress, and autophagy.
研究领域:
兽医学
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药理学
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毒理学
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产品关联
DOI
PubMed
高影响因子
ENVIRONMENTAL SCIENCE & TECHNOLOGY
·
2024
·
IF 10.8
Yanyu Zhou,Qiuli Li,Quan Zhang,Meile Yuan,Xiaoshan Zhu,Yuanchao Li,Qipei Li,Craig A. Downs,Danwei Huang,Loke-Ming Chou,Hongwei Zhao
Global warming has caused the degradation of coral reefs around the world. While stress-tolerant corals have demonstrated the ability to acclimatize to ocean warming, it remains unclear whether they can sustain their thermal resilience when superimposed with other coastal environmental stressors. We report the combined impacts of a photosystem II (PSII) herbicide, prometryn, and ocean warming on the stress-tolerant coral Galaxea fascicularis through physiological and omics analyses. The results demonstrate that the heat-stress-induced inhibition of photosynthetic efficiency in G. fascicularis is exacerbated in the presence of prometryn. Transcriptomics and metabolomics analyses indicate that the prometryn exposure may overwhelm the photosystem repair mechanism in stress-tolerant corals, thereby compromising their capacity for thermal acclimation. Moreover, prometryn might amplify the adverse effects of heat stress on key energy and nutrient metabolism pathways and induce a stronger response to oxidative stress in stress-tolerant corals. The findings indicate that the presence of prometryn at environmentally relevant concentrations would render corals more susceptible to heat stress and exacerbate the breakdown of coral Symbiodiniaceae symbiosis. The present study provides valuable insights into the necessity of prioritizing PSII herbicide pollution reduction in coral reef protection efforts while mitigating the effects of climate change.
研究领域:
海洋生物学
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环境科学
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生态学
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产品关联
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
·
2022
·Vol. 23
·期 20
·12064
·
IF 6.208
Yan Zhou,Yuehan Wang,Chi Teng Vong,Yanyan Zhu,Baojun Xu,Cheng-Chao Ruan,Yitao Wang,Wai San Cheang
Jatrorrhizine (JAT) is one of the major bioactive protoberberine alkaloids found in rhizoma coptidis, which has hypoglycemic and hypolipidemic potential. This study aimed to evaluate the vasoprotective effects of JAT in diabetes and obesity and the underlying mechanism involved. Mouse aortas, carotid arteries and human umbilical cord vein endothelial cells (HUVECs) were treated with risk factors (high glucose or tunicamycin) with and without JAT ex vivo and in vitro. Furthermore, aortas were obtained from mice with chronic treatment: (1) control; (2) diet-induced obese (DIO) mice fed a high-fat diet (45% kcal% fat) for 15 weeks; and (3) DIO mice orally administered JAT at 50 mg/kg/day for the last 5 weeks. High glucose or endoplasmic reticulum (ER) stress inducer tunicamycin impaired acetylcholine-induced endothelium-dependent relaxations (EDRs) in mouse aortas, induced oxidative stress in carotid arteries and HUVECs, downregulated phosphorylations of Akt at Ser473 and eNOS at Ser1177 and enhanced ER stress in mouse aortas and HUVECs, and these impairments were reversed by cotreatment with JAT. JAT increased NO release in high-glucose-treated mouse aortas and HUVECs. In addition, chronic JAT treatment restored endothelial function with EDRs comparable to the control, increased Akt/eNOS phosphorylation, and attenuated ER stress and oxidative stress in aortas from DIO mice. Blood pressure, glucose sensitivity, fatty liver and its morphological change, as well as plasma levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and plasma lipid profile, were also normalized by JAT treatment. Collectively, our data may be the first to reveal the vasoprotective effect of JAT that ameliorates endothelial dysfunction in diabetes and obesity through enhancement of the Akt/eNOS pathway and NO bioavailability, as well as suppression of ER stress and oxidative stress.Keywords:diabetes;endothelial dysfunction;jatrorrhizine;endoplasmic reticulum stress;oxidative stress
研究领域:
药理学
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内分泌学
·
心血管科学
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DOI
PubMed
高影响因子
Clinics
·
2025
·
IF 2.4
Jingwei Liu,Xujie Sun,Junfeng Liang,Shiqiang Song
Introduction Renal Ischemia-Reperfusion Injury (RIRI) often arises due to heightened oxidative stress, rendering it a central focus of research. Sestrin2 plays a pivotal role in regulating oxidative stress; nevertheless, its impact on the renoprotective properties of Eugenol (EU) during RIRI warrants further investigation. Methods Mice and TCMK-1 cells were categorically assigned into six groups: Sham/Control, Ischemia-Reperfusion (IR)/HR (Hypoxia-Reoxygenation), IR/HR+EU, Sham/Control+Sestrin2-KO, IR/HR+Sestrin2-KO, and IR/HR+EU+Sestrin2-KO. The effects of EU and the involvement of Sestrin2 in RIRI/HR were evaluated using Urea Nitrogen (BUN), Creatinine (Scr), Superoxide Dismutase (SOD), Glutathione (GSH), Catalase (CAT), and Malondialdehyde (MDA) assay kits; western blotting; cell viability assays; HE-staining; and Reactive Oxygen Species (ROS) detection. Results Following RIRI/HR, a marked deterioration in kidney function and a significant surge in oxidative stress levels were observed. However, EU treatment ameliorated renal injury and inhibited oxidative stress. Additionally, EU upregulated Sestrin2 expression, and the renoprotective effects of EU were reversed upon Sestrin2 knockdown. Conclusion The present study posits that EU effectively mitigates RIRI/HRI (Hypoxia-Reoxygenation Injury), and its mechanism of renal protection potentially involves the upregulation of Sestrin2, coupled with the inhibition of oxidative and Endoplasmic Reticulum Stress (ERS).
研究领域:
药理学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Antioxidants
·
2023
·Vol. 12
·期 10
·1860
·
IF 7
Hongyan Li,Yanzhi Zeng,Xinyu Zheng,Guangjun Wang,Jingjing Tian,Wangbao Gong,Yun Xia,Kai Zhang,Zhifei Li,Wenping Xie,Jun Xie,Ermeng Yu
To investigate the impact of betaine on high-carbohydrate-diet-induced oxidative stress and endoplasmic reticulum (ER) stress, mandarin fish (Siniperca chuatsi) (23.73 ± 0.05 g) were fed with control (NC), betaine (BET), high carbohydrate (HC), and high carbohydrate + betaine (HC + BET) diets for 8 weeks. The results showed that betaine significantly promoted the growth of mandarin fish irrespective of the dietary carbohydrate levels. The HC diet induced oxidative stress, as evidenced by significantly elevated MDA levels. The HC diet significantly stimulated the mRNA levels of genes involved in ER stress (ire1,perk,atf6,xbp1,eif2α,atf4,chop), autophagy (ulk1,becn1,lc3b), and apoptosis (bax). However, betaine mitigated HC-diet-induced oxidative stress by modulating antioxidant enzymes and alleviated ER stress by regulating the mRNA of genes in the PERK-eIF2a-ATF4 pathway. Additionally, betaine significantly reduced the mRNA levels ofbecn1andbax, along with the apoptosis rate, indicating a mitigating effect on autophagy and apoptosis. Overall, dietary betaine improved growth, attenuated HC-diet-induced oxidative stress and ER stress, and ultimately alleviated apoptosis in mandarin fish. These findings provide evidence for the use of betaine in aquafeeds to counter disruptive effects due to diets containing high carbohydrate levels.Keywords:mandarin fish;high carbohydrate diet;betaine;oxidative stress;ER stress
研究领域:
水产养殖
·
营养学
·
应激生理学
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产品关联
DOI
PubMed
高影响因子
FEBS LETTERS
·
2015
·Vol. 590
·期 1
·22-33
·
IF 3.169
Xue Fu,Xingjie Gao,Lin Ge,Xiaoteng Cui,Chao Su,Wendong Yang,Xiaoming Sun,Wei Zhang,Zhi Yao,Xi Yang,Jie Yang
Malonate, a classic inhibitor of respiratory electron transport chain, induces mitochondrial stress. Stress granules (SGs) are a kind of dynamic foci structure during stress. The study on the connection of mitochondrial stress and SG assembly is still limited. Here, we demonstrated that malonate treatment leads to SG formation and translation inhibition, apart from mitochondrial stress, including enhanced ROS formation, reduced mitochondrial Δψ m and ATP level. The phosphorylation levels of eIF2α and 4EBP1 protein were affected upon mitochondrial dysfunction. However, knockdown of 4EBP1 affected SG formation, rather than eIF2α. In addition, an increase of ATP level under mitochondrial stress enhanced malonate-induced SG aggregation. Overall, malonate stimulation triggers mitochondrial stress and induces the assembly of non-canonical cellular SGs via 4EBP1 pathway.
研究领域:
细胞生物学
·
分子生物学
·
生物化学
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产品关联
DOI
PubMed
高影响因子
Food Bioscience
·
2023
·
IF 5.2
Jiaxin Li,Hengju Ge,Yang Xu,Jiahong Xie,Naymul Karim,Fujie Yan,Jianling Mo,Wei Chen
Chlorogenic acid (CGA) is a phenylpropanoid compound in chrysanthemum, which has a variety of biological activities. Nevertheless, CGA has not yet been studied concerning oxidative stress in hepatocytes. Our research aims to investigate whether chlorogenic acid can improve hepatic oxidative stress, and further illustrated its detailed mechanism. The results of free radicals measurement and Western blot showed that CGA suppressed the activation of JNK (c-Jun NH2-teminal kinase) signaling pathway by ameliorating endoplasmic reticulum stress in H 2 O 2 -treated hepatocytes, thereby eliminating excess intracellular free radicals. In addition, through RT-qPCR, we found that miR-199a-5p down-regulated in H 2 O 2 -induced L02 cells, which was restored by CGA. By inhibiting the expression of miR-199a-5p to promote the transcription of GRP78 gene, the antioxidant capacity of CGA was greatly weakened in hepatocytes. Our findings suggest that CGA treatment alleviated the H 2 O 2 -induced oxidative stress by targeting miR-199a-5p, thereby ameliorating ER stress and inhibiting JNK phosphorylation for antioxidant capacity enhancement. Based on our available results, CGA may be an alternative compound to mitigate hepatic oxidative damage through the miR-199a-5p/GPR78 axis.
研究领域:
药理学
·
分子生物学
·
细胞生物学
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产品关联
DOI
高影响因子
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
·
2022
·
IF 5.785
Dong Li,Wen Cheng,Jiehui Ren,Lu Qin,Xing Zheng,Tian Wan,Min Wang
It is important to study the stress effects and mechanisms of haloacetamide (HAcAm) disinfection byproducts to reveal their health hazards. In this context, toxicological g was applied to evaluate the effects of four HAcAms, revealing the status of gene expression on Escherichia coli in different stress response types (oxidative, protein, membrane, general, DNA). This study revealed that the main toxic action modes of these HAcAms were general and membrane stresses by high-resolution, real-time gene expression profiling combined with clustering analysis. The results of time-gene evaluation showed that the presence of chloroacetamide (CAcAm) and bromoacetamide (BAcAm) generated more reactive oxygen species , thus activating oxidative stress . Trichloroacetamide (tCAcAm) induced altered expression of glutathione marker genes and membrane stress-related genes, and iodoacetamide (IAcAm) caused severe DNA damage by damaging DNA strands and individual nucleotides mainly through damage to nucleic acids and bases. Furthermore, quantitative structure-activity relationship (QSAR) modelling results indicated that the biological activities of HAcAms were related to their quantum chemical and topological properties.
研究领域:
毒理学
·
分子生物学
·
环境科学
·
基因组学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Antioxidants
·
2022
·Vol. 11
·期 10
·2029
·
IF 7.675
Wenrong Feng,Shengyan Su,Changyou Song,Fan Yu,Jun Zhou,Jianlin Li,Rui Jia,Pao Xu,Yongkai Tang
High concentrations of copper (Cu2+) pose a great threat to aquatic animals. However, the mechanisms underlying the response of crustaceans to Cu2+exposure have not been well studied. Therefore, we investigated the alterations of physiological and molecular parameters in Chinese mitten crab (Eriocheir sinensis) after Cu2+exposure. The crabs were exposed to 0 (control), 0.04, 0.18, and 0.70 mg/L of Cu2+for 5 days, and the hemolymph, hepatopancreas, gills, and muscle were sampled. The results showed that Cu2+exposure decreased the antioxidative capacity and promoted lipid peroxidation in different tissues. Apoptosis was induced by Cu2+exposure, and this activation was associated with the mitochondrial and ERK pathways in the hepatopancreas. ER stress-related genes were upregulated in the hepatopancreas but downregulated in the gills at higher doses of Cu2+. Autophagy was considerably influenced by Cu2+exposure, as evidenced by the upregulation of autophagy-related genes in the hepatopancreas and gills. Cu2+exposure also caused an immune response in different tissues, especially the hepatopancreas, where the TLR2-MyD88-NF-κB pathway was initiated to mediate the inflammatory response. Overall, our results suggest that Cu2+exposure induces oxidative stress, ER stress, apoptosis, autophagy, and immune response inE. sinensis, and the toxicity may be implicated following the activation of the ERK, AMPK, and TLR2-MyD88-NF-κB pathways.Keywords:copper;apoptosis;endoplasmic reticulum stress;oxidative stress;Eriocheir sinensis
研究领域:
水生毒理学
·
分子生物学
·
免疫学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）