Biological Trace Element Research最新文献

{"title":"Role of Nitric Oxide, TNF-α and Caspase-3 in Lead Acetate-Exposed Rats Pretreated with Aqueous Rosmarinus officinalis Leaf Extract.","authors":"Adaze Bijou Enogieru, Etinosa Nathan Iyoha","doi":"10.1007/s12011-023-03974-9","DOIUrl":"10.1007/s12011-023-03974-9","url":null,"abstract":"<p><p>Lead (Pb) toxicity is a worldwide significant public health challenge causing several neurological disorders. Reports indicate that plants rich in antioxidants, such as Rosmarinus officinalis (RO), can counteract Pb accumulation and its toxicity in the brain. Due to a dearth of literature evidence demonstrating the protective activity of RO against Pb toxicity, this study investigated such activity in Wistar rats. Thirty-six Wistar rats were allocated into six groups (n=6), namely I (control), II (lead acetate [Pb]; 100 mg/kg b.w.), III (100 mg/kg of RO and 100 mg/kg of Pb), IV (200 mg/kg of RO and 100 mg/kg of Pb), V (100 mg/kg b.w. of RO) and VI (200 mg/kg b.w. of RO). After 28 days, neurobehavioural, antioxidant, lipid peroxidation, apoptotic and inflammatory activities as well as the histology of the cerebellum were evaluated. Body weight, locomotion and exploration as well as antioxidant enzymes were significantly (p < 0.05) decreased in Pb-exposed rats when compared to control. Conversely, lipid peroxidation, nitric oxide, tumour necrosis factor-alpha and caspase-3 activities were significantly (p < 0.05) upregulated in the Pb-exposed rats when compared to control. These parameters were, however, significantly (p<0.05) attenuated in the RO-pretreated rats when compared to Pb-exposed rats. Cerebellar histology of the Pb-exposed rats showed severe degeneration of the Purkinje cells whereas the RO-pretreated rats showed better cerebellar architecture. These findings demonstrate that the neuroprotective activity of RO is facilitated via its effective antioxidant, anti-inflammatory and anti-apoptotic effects.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138443735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zinc-Mediated Endoplasmic Reticulum Stress and Metallothionein Alleviate Arsenic-Induced Cardiotoxicity in Cyprinus Carpio.","authors":"Haiyan Dong, Hongwei Song, Yachen Liu, Hongfei Zou","doi":"10.1007/s12011-023-03975-8","DOIUrl":"10.1007/s12011-023-03975-8","url":null,"abstract":"<p><p>Arsenic (As) is a natural component of the Earth's crust, and its inorganic form is highly toxic. The problem of As pollution in water is extremely urgent, and its impact on aquatic organisms should be widely considered. Here, 120 common carp were selected as the test subjects and were exposed to environmentally relevant concentrations of As (2.83 mg L^- 1) for 30 days. Histomorphological observations showed the adverse effects of As on the heart: irregular arrangement of myocardial fibers, rupture of muscle fiber bundles, inflammatory infiltration, and hemorrhages. Mechanistically, abnormal expression of factors related to As-induced inflammation (TLR4/MYD88/NF-κB pathway), endoplasmic reticulum stress (CHOP, GRP78, ATF6, PERK, IRE1) and oxidative stress (SOD, CAT, Nrf2, HO-1) was observed. Then, we tried to find a protective agent against As-induced myocardial injury. As one of the important metal elements for maintaining cell growth and immunity, zinc (Zn, 1 mg L^- 1) significantly alleviated the pathological abnormalities induced by As, and the changes in physiological and biochemical indices in response to As exposure were significantly alleviated by Zn administration, which was accompanied by the restoration of metallothionein (ZIP8, Znt1, Znt5, Znt7) and heat shock protein (HSP60, HSP70, HSP90) expression. These results suggest for the possibilty of developing Zn as a candidate therapeutic agent for As induced aquatic toxicology.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138457652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association Between Dietary Zinc Intake and Increased Renal Function in US Adults.","authors":"Chang Liu, Hao Zhang, Yuwei Yang, Yan Cao, Dan Liang","doi":"10.1007/s12011-023-03969-6","DOIUrl":"10.1007/s12011-023-03969-6","url":null,"abstract":"<p><p>We aimed to investigate the association between the dietary zinc intake and the risk of albuminuria, low estimated glomerular filtration rate (eGFR), and chronic kidney disease (CKD) in the US general population. This study was a cross-sectional study utilizing the data from the 2003-2018 National Health and Nutrition Examination Survey. Albuminuria was defined as urinary albumin:creatinine ratio (ACR) > 30 mg/g. Low eGFR was defined as an eGFR of less than 60 mL/min/1.73 m². CKD is characterized by albuminuria or low eGFR. Multivariate logistic regression analysis, subgroup analyses, interaction tests, and restricted cubic spline (RCS) analysis were performed in this study. For 37,195 enrolled participants in this study, the mean dietary zinc intake was 11.85 ± 0.07 mg/day, and the rate of albuminuria, low eGFR, and CKD was 9.37%, 6.68%, and 14.10%, respectively. Participants with a higher dietary zinc intake showed a lower risk of albuminuria, low eGFR, and CKD. In the fully adjusted model, we found that participants in the highest dietary zinc intake quartile had 26% lower odds of the rate of CKD than those in quartile 1. Subgroup analyses showed that dietary zinc intake was positively associated with the risk of low eGFR in participants who were now smokers. The potential nonlinear relationship between dietary zinc intake and the risk of CKD and albuminuria was also revealed. Higher dietary zinc intake was significantly associated with a lower likelihood of CKD, which might be helpful in kidney function protection among the general population.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138443733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"p53-Mediated Mitochondrial Translocation of EI24 Triggered by ER Stress Plays an Important Role in Arsenic-Induced Liver Damage via Activating Mitochondrial Apoptotic Pathway.","authors":"Chunyan Liu, Aihua Zhang","doi":"10.1007/s12011-023-03967-8","DOIUrl":"10.1007/s12011-023-03967-8","url":null,"abstract":"<p><p>Chronic arsenic poisoning is a public health problem worldwide. In addition to skin lesions, the detrimental effect of arsenic poisoning on liver damage is one of the major issues. Our previous studies demonstrated that endoplasmic reticulum (ER) stress and p53 were associated with arsenic-induced liver damage. Literature has shown that EI24 is involved in hepatocyte hypertrophy; however, the underlying role and mechanism in arsenic-induced liver damage have not been fully elucidated. In this study, we explored the role of ER stress, p53, and EI24 as well as the regulatory relationship in arsenic poisoning populations and L-02 cells treated with distinct concentration NaAsO₂ (2.5, 5, 10, and 20 μM). Results showed that as with arsenic dose increment, expression levels of ER stress key proteins GRP78, ATF4, and CHOP were significantly enhanced. Additionally, p53 expression in nucleus, p53 phosphorylation at Ser15 and Ser1392, and p53 acetylation at lys382 were significantly increased in NaAsO₂-treated L-02 cells. ER stress inhibitor 4-phenylbutyric acid (4-PBA) decreased the expression of p53 phosphorylation at Ser 392, p53 acetylation at lys382, and p53 expression in nucleus. Additionally, in 5 μM NaAsO₂ condition, p53 inhibitor pifithrin-α (PFT-α) aggravated 5 μM NaAsO₂-induced GRP78, ATF4, and CHOP expressions, cell apoptosis, and protein-SH consumption. But in 20 μM NaAsO₂ condition, PFT-α attenuated NaAsO₂-induced cell apoptosis. Further results showed that 20 μM NaAsO₂ facilitated translocation of EI24 from ER to mitochondrion and interaction with VDAC2, leading to activate mitochondrial apoptotic pathway, but not observed in the 5-μM NaAsO₂ group. Moreover, PFT-α and 4-PBA inhibited 20 μM NaAsO₂-induced EI24 expression in mitochondrion. Collectively, our results indicated that arsenic induced p53 activation via ER stress, under relatively low NaAsO₂ concentration, NaAsO₂-triggered p53 activation protected cells from apoptosis by alleviating ER stress. Another finding was that under relatively high NaAsO₂ concentration, NaAsO₂-activated p53 facilitated EI24 mitochondrial translocation and caused mitochondrial permeability increase, which represented a switch of p53 from a benefit role to pro-apoptosis function in NaAsO₂-treated cells. The study contributed to in-depth understanding the mechanism of arsenic-induced liver damage and providing potential clues for following study.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138450792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dispersive Solid-phase Microextraction of Lead in Waters and Edible Lettuce and Dill Extracts in the Unified Bioaccessibility Method (UBM) Saliva Solution.","authors":"Şerife Tokalıoğlu, Shukria Shahir, Ebru Tekneci Akgül, Bahire Filiz Şenkal","doi":"10.1007/s12011-023-04001-7","DOIUrl":"10.1007/s12011-023-04001-7","url":null,"abstract":"<p><p>A new thiosemicarbazide-modified, sulfonamide-based poly (styrene) adsorbent (T-CSPS) was prepared starting from the reaction of chlorosulfonated polystyrene and thiosemicarbazide. It was characterized by SEM-EDX, FT-IR, and zeta potential. The T-CSPS was used as an adsorbent for the first time for the dispersive solid-phase microextraction (d-SPµE) and preconcentration of Pb(II) ions from waters and dill and lettuce extracts in the unified bioaccessibility method (UBM) saliva. Lead was then determined using the FAAS. In the first step of optimization, the solution pH was changed from 2 to 8, and pH 4 with a recovery value of 103% ± 5 was selected. Two milliliters of 2 mol L^-1 HCl was chosen as eluent. Contact times were found to be only 2 min. Effects of coexisting ions and sample volume were tested. Under optimal conditions, the preconcentration factor (PF) and the adsorption capacity were 15 and 40 mg g^-1. The RSD% was 2.2% and 3.1% for intra-day and inter-day precision, respectively. The LOD and LOQ were found to be 5.1 µg L^-1 and 16.9 µg L^-1, respectively. The accuracy of the d-SPµE was checked by TMDA-70.2 Lake water and BCR-482 Lichen-certified reference materials and also applying d-SPµE to spiked waters and lettuce and dill extracts in UBM saliva.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138797111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Boric Acid Improved Cryopreserved Mouse Embryo Development.","authors":"A Kocabay, A C Taskin","doi":"10.1007/s12011-023-03990-9","DOIUrl":"10.1007/s12011-023-03990-9","url":null,"abstract":"<p><p>Boric acid (BA) is an essential trace element that is required to support the metabolic pathways in plants, humans, and animals. The present study investigates the in vitro development and quality of single-cell mouse embryos in a BA-added culture medium after cryopreservation using the solid-surface vitrification method. For this purpose, the pronuclear-stage embryos derived from superovulated C57Bl/6j mouse strains and the one-cell embryos were then cryopreserved using the solid-surface vitrification (SSV) method. After thawing, the embryos were cultured in a BA-added medium at 37 °C in a 5% CO₂ environment until the blastocyst stage. The resulting in vitro development rates of the embryos in the control group, SSV group, and SSV + 1.62 × 10^-4 μM BA group were 68.11% (36/59), 40.16% (16/48), and 64.92% (28/48) respectively, indicating that the BA supported the in vitro development of the embryos cryopreserved using the SSV method. Our results suggest that the addition of boric acid to the culture media increased the development rate of the embryos that were vitrified using the SSV method.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138481808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Signal Transduction Associated with Mn-induced Neurological Dysfunction.","authors":"Xiao-Wei Zheng, Yuan-Yuan Fang, Jun-Jie Lin, Jing-Jing Luo, Shao-Jun Li, Michael Aschner, Yue-Ming Jiang","doi":"10.1007/s12011-023-03999-0","DOIUrl":"10.1007/s12011-023-03999-0","url":null,"abstract":"<p><p>Manganese (Mn) is a heavy metal that occurs widely in nature and has a vital physiological role in growth and development. However, excessive exposure to Mn can cause neurological damage, especially cognitive dysfunction, such as learning disability and memory loss. Numerous studies on the mechanisms of Mn-induced nervous system damage found that this metal targets a variety of metabolic pathways, for example, endoplasmic reticulum stress, apoptosis, neuroinflammation, cellular signaling pathway changes, and neurotransmitter metabolism interference. This article reviews the latest research progress on multiple signaling pathways related to Mn-induced neurological dysfunction.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139058121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of BNIP3 and Blocked Autophagy Flux in Arsenic-Induced Oxidative Stress-Induced Liver Injury in Rats.","authors":"Haiyan Zhi, Dingnian Bi, Dan Zheng, Qingyue Lu, Hongling Wang, Yi Wang, Ying Lv, Didong Lou, Yong Hu","doi":"10.1007/s12011-023-03982-9","DOIUrl":"10.1007/s12011-023-03982-9","url":null,"abstract":"<p><p>Arsenic is a widely distributed environmental toxic substance in nature. Chronic arsenic exposure can cause permanent damage to the liver, resulting in the death of poisoned patients. However, the mechanism of liver damage caused by arsenic poisoning is yet unclear. Here, four different concentrations of sodium arsenite (NaAsO₂) (0 mg/L (control group), 25 mg/L, 50 mg/L, and 100 mg/L group)were established to induce liver injury in rats. Taking this into account, the relationship and potential mechanisms of oxidative stress, Bcl-2/adenovirus E1B-19-kDa-interacting protein 3 (BNIP3), and inhibition of autophagy flux in liver injury caused by arsenic poisoning were studied. The results indicated that long-term exposure to NaAsO₂ could induce oxidative stress, leading to high expression of BNIP3, thereby impaired autophagy flux, and ultimately resulting in liver damage. This research provides an important basis for future research on liver damage caused by chronic arsenic exposure and prevention and treatment with BNIP3 as the target.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138476697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic Iodine Intake Excess Damages the Structure of Articular Cartilage and Epiphyseal Growth Plate.","authors":"Ying Zhang, Xin Zhao, Le Shan, Miao Liu, Zixuan Zhang, Zeji Wang, Xinbao Zhang, Haohao Meng, Yan Song, Wanqi Zhang, Zhongna Sang","doi":"10.1007/s12011-023-03985-6","DOIUrl":"10.1007/s12011-023-03985-6","url":null,"abstract":"<p><p>This study aimed to explore the influence of excess iodine on the articular cartilage and epiphyseal growth plate in rats. Wistar rats (n = 200) were randomly divided into five groups with 40 rats in each: normal iodine (NI), 5-fold high iodine group (5HI), 10-fold high iodine group (10HI), 50-fold high iodine group (50HI), and 100-fold high iodine group (100HI). The rats were executed in 6 and 12 months. 24-h urinary iodine concentration (UIC) was monitored by arsenic-cerium catalytic spectrophotometry. The chemiluminescence method was used to determine the thyroid function. The pathological changes in the epiphyseal plate, articular cartilage, and thickness of the epiphyseal plate were observed. The mRNA expression of collagen II (ColII), collagen X, matrix metalloproteinase-13 (MMP-13), and fibroblast growth factor receptor 1 in articular chondrocytes was detected by RT-PCR. 24-h UIC increased as iodine intake increased. In the 12th month, there was a significant increase in serum sTSH and a decrease in serum FT₄ in HI groups, compared to the NI group. There was a decrease in the number of proliferating cells in the epiphyseal plate and an increase in the number of mast cell layers. The chondrocytes appeared disorganized, and the tidal lines were disturbed or even broken. Growth plate thickness decreased with increasing iodine intake. Compared with the NI group, ColII and MMP-13 mRNA expression in chondrocytes in all HI groups significantly increased. Chronic iodine overdose increases the risk of hypothyroidism. Chronic iodine overdose leads to abnormal morphology of epiphyseal growth plates and articular cartilage, increasing the risk of osteoarthritis.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138497738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Chlorella vulgaris in Attenuating Infertility Induced by Cadmium Chloride via Suppressing Oxidative Stress and Modulating Spermatogenesis and Steroidogenesis in Male Rats.","authors":"Mayada R Farag, Nesma I El-Naseery, Eman I El Behery, Doaa S Nouh, Amany El-Mleeh, Ismail M A Mostafa, Mahmoud Alagawany, Alessandro Di Cerbo, Mahmoud M Azzam, Suzan A Mawed","doi":"10.1007/s12011-023-03971-y","DOIUrl":"10.1007/s12011-023-03971-y","url":null,"abstract":"<p><p>Cadmium (Cd) is an environmental pollutant known as endocrine disruptor . Cd has been reported to induce perturbations of the testicular functions and the subsequent decline of the male fertility of both animals and humans. Chlorella vulgaris (ChV) a species of green microalga has been reported to have multiple beneficial activities such as anti-inflammatory, antioxidant, and antiapoptotic effects. Thus, this work was conducted to declare the benefits of Chlorella vulgaris (ChV) (500 mg/kg doses) against cadmium chloride CdCl₂ (2 mg/kg doses) toxicity on the main and accessory reproductive organs' weight, structure, and function of male rats. Briefly, 40 adult male rats in 4 groups (n = 10) were used as follows; control, ChV, CdCl2, and CdCl2+ChV. (i) The 1st group was kept as control fed on pellet chow and water ad libitum. (ii) The second group is Chlorella vulgaris (ChV) group fed with C. vulgaris alga for 10 days (500 mg/kg BW). (iii) The third group was administrated CdCl₂ (2mg/kg BW) via subcutaneous injection (S/C) daily for 10 days. (iv) The fourth group administered both CdCl₂ and ChV with the abovementioned doses daily for successive 10 days. Our observations declared that cadmium exhibited an adverse influence on the testes and prostate gland architecture indicated by seminiferous tubule destruction, testicular edema, degeneration of Leydig cells, and prostate acini damage. All together affect the epididymal semen quality and quantity including sperm viability, motility, and count. Interestingly, ChV could restore the testicular architecture and spermatozoa regeneration accompanied by semen quality improvement and increased reproductive hormones including testosterone. On the other side, ChV suppresses reactive oxygen species (ROS) formation via enhancement the antioxidant-related genes in the testicular tissue including SOD, CAT, GSH, and MDA and maintaining spermatocyte survival via suppression of apoptotic related genes including caspase3 and activating steroidogenic related genes including StAR and HSD17β3 in the cadmium-treated testes. In this study, ChV could enhance male fertility under normal or stressful conditions and ameliorate the adverse effects of hazardous heavy metals that are widely distributed in our environment.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138797117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}