SCIENCE OF THE TOTAL ENVIRONMENT
·
2022
·
IF 10.753
Junzhao Yuan,Xiaoqian Huang,Jianhong Gu,Yan Yuan,Zongping Liu,Hui Zou,Jianchun Bian
Cadmium (Cd) pollution in environment is toxic to birds. This study aimed to assess antagonistic effect of honokiol (HNK) on Cd-induced quail ( Coturnix japonica ) liver tissue damage and Cd-induced vacuolation in hepatocytes. We found that HNK alleviated Cd-induced liver pathological damage marked by elevated serum liver biochemical indicators, disordered antioxidant levels and trace elements in quails. HNK reduced Cd-induced liver cell apoptosis as assessed by western blotting and TUNEL staining. The ultrastructure of hepatocytes under transmission electron microscope revealed that Cd induced mitochondrial damage in addition to abnormal enlargement and increased vacuolar structure of cells. Mitochondrial damage and vacuolization were reduced in the HNK + Cd group. Cd induced an increase in the levels of endosomal/lysosomal-related genes, while HNK treatment reversed this effect. Finally, we demonstrated that vacuolation in buffalo rat liver 3A (BRL 3A) cells occurred primarily due to Cd-induced oxidative stress damage that reduces mitochondrial ATP content and indirectly led to dysfunction of ATP-dependent lipid kinase PIKfyve complex. In summary, we are the first to report that Cd induces abnormal enlargement of endosome/lysosomes in quail liver cells and HNK alleviated this phenomenon by reducing mitochondrial damage and increasing intracellular ATP level. This study demonstrated the toxic effect of Cd pollution on birds and how HNK mitigated these effect at the cellular level. Overall, more research on Cd pollution and HNK use in animal husbandry is warranted.
研究领域:
环境毒理学
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分子生物学
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动物生理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CHEMOSPHERE
·
2018
·
IF 4.427
Peng-Cheng Li,Xue-Nan Li,Zheng-Hai Du,Hui Wang,Zhuo-Ran Yu,Jin-Long Li
Di (2-ethyl hexyl) phthalate (DEHP) as a plasticizer can leach away from the plastic and hence entrances into the animal food chain which caused serious hazard in organs of animals, but there are few studies on DEHP kidney toxicity. The heat-shock response (HSR) consisting of the HSPs and HSFs plays an important role in various toxicity stress conditions. To investigate the influence on kidney toxicity and the modulation of HSR during DEHP exposure, female quail were fed the diet with 0, 250, 500 and 750 mg/kg DEHP by gavage administration for 45 days. The shrinkages of glomeruli and dilation of kidney tubule epithelia cells were observed in the kidney of DEHP-exposed quail. DEHP treatment could significantly decrease the expressions of HSP25, HSP27, HSP47, HSP60 , while the expressions of HSP10, HSP40, HSP70, HSP90, HSP110 were upregulated in the kidney. In addition, the expression levels of HSF1 and HSF3 were significantly increased under DEHP. This is the first study to demonstrate quail exposure to DEHP is in fact detrimental to bird kidney. Besides, DEHP could attack HSR by affecting the synthesis of HSFs to mediate the transcription of the HSPs resulting in kidney damage.
研究领域:
毒理学
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ENVIRONMENTAL POLLUTION
·
2018
·
IF 4.358
Yi Zhao,Zheng-Hai Du,Milton Talukder,Jia Lin,Xue-Nan Li,Cong Zhang,Jin-Long Li
The widely used Di-(2-ethylhexyl) phthalate (DEHP) has been reported to exhibit ubiquitous environmental and global health hazards. The bioaccumulation and environmental persistence of DEHP can cause serious health hazards in wildlife animals and human. However, DEHP-induced nephrotoxicity in bird is remained unknown. Thus, this study explored the related mechanism of DEHP nephrotoxicity in quail. For this purpose, quail were exposed with DEHP at doses of 0, 250, 500, and 1000 mg/kg body weight daily by gavage administration for 45 days. The results showed that DEHP exposure induced renal injury, oxidative stress , and endoplasmic reticulum (ER) degeneration. Low level DEHP (250 mg/kg) exposure inhibited Nrf2 signaling pathway and induced renal injury via oxidative stress and suppressed the unfolded protein response (UPR) signaling pathway and induced ER stress in the kidney. But surprisingly, high level DEHP (500 mg/kg and 1000 mg/kg) exposure activated Nrf2 and UPR signaling pathways and protected kidney, but they still couldn't resist the toxicity of DEHP. Our study demonstrated that DEHP-induced nephrotoxicity in quail was associated with activating Nrf2-mediated antioxidant defense response and UPR signaling pathway.
研究领域:
毒理学
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环境科学
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分子生物学
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动物生理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Food Production Processing and Nutrition
·
2024
·Vol. 6
·期 1
·1-15
·
IF 4
Zhou Zheng,Jiang Haonan,Sun Haoyuan,Huang Xu-Hui,Cui Shuang,Zhou Dayong,Qin Lei
After thermal treatment, quail eggs pruduce an attractive flavor that is favored by consumers. In this study, the key aroma volatiles and their lipid precursors during thermal treatment were investigated by the electronic nose, GC-MS, GC-O-MS and UPLC-Q-Exactive HF-X. The results exhibited that the raw and fresh flavor of raw egg yolks came from 1-Octen-3-ol, 2-Ethyl-1-hexanol, 1-Decene, and 1-Undecene. 2-Methyl-3-octanone, Toluene, and some aromatic compounds worked synergistically to contribute to the aroma profile of boiled eggs. (+)-2-Bornanone, Octanal, 2-Methyl-butanal, Nonanal, (.+Dihydro-3-hydroxy-4,4-dimethyl-2(3 H)-furanone, 6,7-Dihydro-2,5-dimethyl-5 H-cyclopentapyrazine, (E)-2-methyl-6-(1-propenyl)-pyrazine, 2-Ethyl-3,5-dimethyl-pyrazine, 3,5-Diethyl-2-methyl-pyrazine, 2,5-Dimethyl-pyrazine were the key flavor compounds in the fried egg and gave it the popcorn and roasted flavors. The statistical analysis of the lipid profile revealed that brief, high-temperature heating (100 or 200 °C for 10 min) in typical boiled and fried quail eggs had minor effects on the lipid nutritional value. PE-related lipids, particularly those containing 18-carbon fatty acids, contributed to the aroma formation of fried quail eggs. Graphical Abstract
研究领域:
食品科学
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分析化学
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营养学
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产品关联
DOI
高影响因子
ENVIRONMENTAL POLLUTION
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2017
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IF 5.099
Zheng-Hai Du,Jun Xia,Xiao-Chen Sun,Xue-Nan Li,Cong Zhang,Hua-Shan Zhao,Shi-Yong Zhu,Jin-Long Li
Di-(2-ethylhexyl)-phthalate (DEHP) is causing serious health hazard in wildlife animal and human through environment and food chain, including the effect of brain development and impacted neurobehavioral outcomes. However, DEHP exposure caused cerebellar toxicity in bird remains unclear. To evaluate DEHP-exerted potential neurotoxicity in cerebellum, male quails were exposed with 0, 250, 500 and 750 mg/kg BW/day DEHP by gavage treatment for 45 days. Neurobehavioral abnormality and cerebellar histopathological alternation were observed in DEHP-induced quails. DEHP exposure increased the contents of total Cytochrome P450s (CYPs) and Cytochrome b5 (Cyt b5) and the activities of NADPH-cytochrome c reductase (NCR) and aniline-4-hydeoxylase (AH) in quail cerebellum. The expression of nuclear xenobiotic receptors (NXRs) and the transcriptions of CYP enzyme isoforms were also influenced in cerebellum by DEHP exposure. These results suggested that DEHP exposure caused the toxic effects of quail cerebellum. DEHP exposure disrupted the cerebellar CYP enzyme system homeostasis via affecting the transcription of CYP enzyme isoforms. The cerebellar P450arom and CYP3A4 might be biomarkers in evaluating the neurotoxicity of DEHP in bird. Finally, this study provided new evidence that DEHP-induced toxic effect of quail cerebellum was associated with activating the NXRs responses and disrupting the CYP enzyme system homeostasis.
研究领域:
环境毒理学
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神经毒理学
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
FOOD CHEMISTRY
·
2024
·
IF 8.5
Huan Liu,Yuping Zhang,Hengbin Ji,Junke Li,Qianli Ma,Nazimah Hamid,Jiangtao Xing,Peng Gao,Pi Li,Jianxun Li,Qianqian Li
Lipids play a significant role in aroma formation. However, lipid variations and their impact on aroma during the processing of quail meat remain unknown. Therefore, a comprehensive analysis of lipids and aroma compounds was conducted in circulating non-fried roasted quail meat. Nineteen odorants were identified as key aroma compounds in the roasted quail meat at 40 min with OAVs of >1. The concentrations of most key odorants significantly increased in circulating non-fried roasted (CNR) quail meat within the first 30 min of roasting, reaching maximum values at 40 min. Phospholipids, neutral lipids, and sphingolipids emerged as potential markers for distinguishing different samples. Neutral lipids had the highest peak areas and significantly contributed to the aroma retention. Phospholipids and neutral lipids with unsaturated fatty acids, particularly C 18 acyl groups, played a crucial role in aroma formation. This study provides valuable insights into the role of lipids in determining aroma quality.
研究领域:
食品科学
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生物化学
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产品关联
DOI
PubMed
高影响因子
Journal of Veterinary Science
·
2025
·Vol. 26
·期 4
·e34
·
IF 1.5
ShaoJun Zheng,YaQin Bu,Sheng Li,NaiDong Chen
Importance Hyperuricemia (HUA) is a major metabolic disorder in poultry, leading to gout and kidney damage, which affects farm productivity. Accordingly, understanding the pharmacodynamics (PD) and pharmacokinetics (PK) of uric acid-lowering drugs is essential for improving the treatment strategies in poultry. Objective This study examined the PD and PK characteristics of allopurinol and benzbromarone, two uric acid-lowering drugs, in a quail model of HUA. Methods A hyperuricemic quail model was established using a high-purine diet. Allopurinol and benzbromarone were administered orally. Blood samples were taken and analyzed for the drug concentrations using high-performance liquid chromatography. Pathological examinations were conducted to assess kidney damage. Results Both drugs lowered the serum uric acid levels. On the other hand, the allopurinol treatment exhibited lower urea and creatinine levels than benzbromarone, indicating potential advantages in reducing kidney damage. Consistent with these findings, the pathological examinations revealed more pronounced kidney damage in the benzbromarone-treated group than in the allopurinol group. PK analysis showed that allopurinol exhibited faster absorption and elimination kinetics than benzbromarone. Both drugs showed a wide distribution in various tissues, with allopurinol and its active metabolite displaying higher excretion levels. Conclusions and Relevance This paper reports the absorption, distribution, metabolism, and excretion processes of allopurinol and benzbromarone in a quail model of HUA. These findings help better understand the PK characteristics of these drugs and promote the use of high uric acid therapy in poultry. In addition, this quail model is a valuable tool for future research on HUA and drug interventions.
研究领域:
兽医学
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药理学
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代谢疾病
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家禽健康
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药物代谢
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
·
2022
·
IF 5.785
Tian-Ning Yang,Xue-Nan Li,Xiao-Wei Li,Jin-Yang Li,Yue-Qiang Huang,Jin-Long Li
As a plasticizer , di-2-ethylhexyl phthalate (DEHP) has been listed as a potential endocrine disruptor by The World Health Organization. The toxicity of DEHP has been widely studied, but its toxicity on the digestive tract of birds has not been clarified. Female quail were treated by gavage with DEHP (250, 500, 750 mg/kg), with the blank and vehicle control groups reserved. The result showed that DEHP raised the damage severity grade, and decreased the ratio of villus length to crypt depth. The content and activity of cytochrome P450 system (CYP450s) were increased by DEHP. DEHP interfered with the transcription of nuclear xenobiotic receptors (NXRs), CYP isoforms, and the nuclear factor-E2-related factor 2 (Nrf2) signaling pathway. This study revealed DEHP could cause the imbalance in CYP450s mediated by NXRs, and then promote Nrf2 mediated antioxidant defense. This study provided new evidence about the mechanisms of DEHP-induced toxic effects on digestive tract.
研究领域:
毒理学
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鸟类生物学
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环境科学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
FOOD AND CHEMICAL TOXICOLOGY
·
2022
·
IF 5.572
Hao Zhang,Yi Zhao,Jia-Gen Cui,Xue-Nan Li,Jin-Long Li
Di(2-ethylhexyl) phthalate (DEHP) is a plasticizer widely used in agricultural and industrial plastic products. Many researchers have demonstrated that DEHP can cause varying degrees of harm to the heart. This research investigated the mechanism by which DEHP causes heart damage in quail. The quail were treated with DEHP (250 mg/kg BW/day, 500 mg/kg BW/day or 750 mg/kg BW/day) for 45 days. The present study suggested that DEHP could cause varying levels of heart damage, including disordered myocardial fiber arrangements, myocardial fiber breakage and myocardial cell swelling. The results showed that DEHP induced mitochondrial damage, such as cavitation lesions and mitochondrial crest breakage. DEHP damaged mitochondria and inhibited nuclear respiratory factor 1 (Nrf1)-mediated mitochondrial biogenesis, which led to mitochondrial damage. DEHP caused oxidative stress in the heart and activated the defense mechanism of the nuclear factor red blood cell 2 related factor 2 (Nrf2) system. DEHP-induced mitophagy was related to a decline in mitochondrial biogenesis and disordered mitochondrial dynamics. The data indicated that DEHP exposure damaged cardiac mitochondria and caused mitophagy and cardiotoxicity. Of note, this study showed that DEHP-induced mitophagy and mitochondrial damage are associated with the dysregulation of mitochondrial biogenesis.
研究领域:
毒理学
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心脏病学
·
分子生物学
✓ 已验证
DOI
PubMed
高影响因子
CHEMOSPHERE
·
2018
·
IF 4.427
Hui Wang,Xue-Nan Li,Peng-Cheng Li,Wei Liu,Zheng-Hai Du,Jin-Long Li
Di(2-ethylhexyl) phthalate (DEHP) is an omnipresent environmental pollutant with endocrine disrupting properties. As a plasticizer , DEHP can be leach from the plastic to transfer the external environment and thus enters the animal food chain, causing serious damage to the animal organs. The heat-shock response (HSR) comprising heat-shock protein (HSPs) and heat-shock transcription factor (HSFs) plays a pivotal role in various toxic stress conditions. For the sake of investigating the effects of DEHP exposure on cardiac toxicity and the regulation of HSR, male quail were fed the diet with 0, 250, 500 and 750 mg/kg DEHP by gavage administration for 45 days. Histopathological changes including cardiomyocyte swelling and muscle fiber dilatation were observed in the hearts exposed to DEHP. During the DEHP treatment, the mRNA expression of HSP60 and HSP70 were universally reduced, while the expression of other HSPs ( HSP10, HSP25, HSP27, HSP40, HSP47, HSP90, HSP110 ) had different degrees of growth. In addition, the levels of HSF1, HSF2, and HSF3 were significantly increased. Given the facts above, DEHP exposure induced the toxic effects of quail heart. DEHP exposure did great harm to HSR via affecting the synthesis of HSFs to mediate the transcription of the HSPs. Ultimately, this study provided new evidence that DEHP-induced cardiotoxicity in quail was related to activation of HSR and playing a protective role.
研究领域:
环境毒理学
·
分子生物学
·
心脏病学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
FOOD AND CHEMICAL TOXICOLOGY
·
2022
·
IF 5.572
Yue-Qiang Huang,Yi-Xi Tang,Bai-Hao Qiu,Milton Talukder,Xue-Nan Li,Jin-Long Li
Di-2-ethylhexyl phthalate (DEHP) has been widely used in many fields (agricultural products, medical instruments, and food packing). As an environmental contaminant, DEHP has a negative impact on human and animal health, and thus toxicity caused by DEHP is increasingly serious health concern. Nevertheless, DEHP-induced liver damage in quail remains unclear. To investigate the mechanism of liver damage caused by DEHP, male quail were treated with DEHP (250, 500, and 750 mg/kg) by gavage. Notably, DEHP exposure results in increased blood lipids and the accumulation of triglycerides (TG), total cholesterol (TC), and non-esterified fatty acid (NEFA) in the liver. Histopathological analysis showed that steatosis and inflammatory cell infiltration were observed in the liver tissue of quails exposed to DEHP. The results of Oil Red O staining displayed that DEHP induced lipid storage in the liver. Moreover, DEHP induced lipid metabolism disorders by activating the LXR / SREBP-1c and PPARα / γ signaling pathway. DEHP exposure obviously caused the up-regulation of pro-inflammatory cytokines ( NF-κB , IL-6 , IL-8 , IL-1β , and TNF-a ). This study showed that DEHP could induce lipid metabolism disorders and inflammatory response via LXR / SREBP-1c / PPARα / γ and NF-κB signaling pathways.
研究领域:
毒理学
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环境健康
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分子生物学
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病理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2022
·
IF 5.195
Yu Wang,Zhi-jian Lin,Jing Huang,Meng-zhen Chu,Xue-li Ding,Wen-jing Li,Qiu-yue Mao,Bing Zhang
Ethnopharmacological relevance Shenling Baizhu San (SLBZ) is a famous Traditional Chinese Medicine (TCM) formula that strengthens the spleen for replenishing qi, removing dampness, and inducing diuresis to relieve diarrhea. Combining the TCM interpretation that dampness is a vital pathogenesis factor in hyperuricemia occurrence and development, SLBZ has excellent potential against hyperuricemia from the perspective of TCM theories. Aim of the study This study aimed to investigate the efficacy of SLBZ against hyperuricemia and its possible mechanism with emphasis on the active components and the core targets. Materials and methods In the present study, we employed meta-analysis and a hyperuricemia quail model to evaluate the uric acid-lowering effect of SLBZ. Bodyweight, serum uric acid , and excreta uric acid levels in quails were assessed. Subsequently, we analyzed the potential active components and core targets of SLBZ against hyperuricemia by network pharmacology and calculated their interaction using molecular docking. Furthermore, the hyperuricemia rats treated with interfering agents of core targets were established to determine the central role of selected targets in hyperuricemia progression. Besides, we isolated and characterized the primary renal tubular epithelial cells of quails to verify the active components and core targets of SLBZ against hyperuricemia. Western blotting was used to observe the expression of core targets treated with active components under the stimulation of interfering agents. Results Data from meta-analysis and animal experiments showed that SLBZ could work effectively against hyperuricemia. Hyperuricemia quails treated with SLBZ displayed significantly reduced serum uric acid levels accompanied by increased excretion of uric acid. According to network pharmacology and molecular docking results, 34 potential active components and the core target peroxisome proliferator-activated receptor gamma (PPARγ) for SLBZ against hyperuricemia were identified. The decreased serum uric acid levels in hyperuricemia rats treated with rosiglitazone , an agonist of PPARγ, confirms the essential role of PPARγ in the pathological process of hyperuricemia. Moreover, we first successfully isolated and characterized the primary renal tubular epithelial cells of quails and observed enhanced phosphorylation of PPARγ at Ser273 in cells handled with high-level uric acid. Whereas, the enhanced expression of p-PPARγ Ser273 could be down-regulated by luteolin and naringenin , two active components of SLBZ against hyperuricemia. Conclusion In summary, SLBZ is a promising anti-hyperuricemia agent, and luteolin and naringenin are the active components for SLBZ against hyperuricemia by down-regulating phosphorylation of PPARγ at Ser273.
研究领域:
药理学
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民族药理学
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网络药理学
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分子生物学
✓ 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）