Quercetin (QE) is a natural flavonoid compound with various biological activities such as antioxidant, antiinflammatory, and detoxification. The use of 17 alpha-methyltestosterone (MT) in aquaculture poses environmental risks. However, it's unknown if QE can prevent MT-induced liver-heart axis toxicity. Therefore, this study utilized five-month-old female Gobiocypris rarus as experimental material, established MT exposure models and QE treatment models, and analyzed indicators related to lipid metabolism, oxidative stress, and inflammation in liver and heart tissues through various methods, including H&E staining, biochemical test, and qRT-PCR. The results showed that MT exposure led to significant pathological changes in hepatocytes and cardiomyocytes, and disordered the levels of TG, FFA, TBA, and CAT in the liver. QE intervention could successfully reduce oxidative damage, tissue damage, and metabolic imbalances.MT exposure resulted in a notable upregulation of genes associated with inflammatory injury markers, including cytokeratin-18 (CK-18) and pro-inflammatory cytokines such as IL-1 beta, IL-6, and TNF-alpha. Quercetin (QE) treatment demonstrated significant immunomodulatory effects. Under H-QE conditions, there was a significant reversal or alleviation of the abnormal expression of these genes. RNA-seq analysis of cardiac tissue indicated that MT interfered with pathways associated with the cytoskeleton, metabolism, and immune response. H-QE demonstrated hepatocardiac-axis protective effects through the modulation of pathways related to cell cycle regulation, lipid metabolism, detoxification processes, and immune homeostasis. This study illustrates that QE can effectively reduce MT-induced hepatocardiac-axis toxicity, showing significant protective potential.

This study investigated the individual and combined effects of Polystyrene microplastics (PS) and 17α-methyltestosterone (MT) on the gill and liver of Gobiocypris rarus.Exposure to PS (0.5 mg/L) and MT (50 ng/L) induced significant histopathological alterations and immunotoxicity. Tissues exhibited inflammatory infiltration, nuclear dissolution, and cytoplasmic vacuolation, with the most severe lesions observed under combined exposure. Gene expression analysis revealed significant upregulation of immune and oxidative stress-related genes, including caspase 6 (CASP6), interleukin-1 receptor type I (IL-1RI), NADPH oxidase 1 (NOX1), Toll-like receptor 2 (TLR-2), and C-C motif chemokine receptor 7 (CCR7), while antioxidant enzyme activities and malondialdehyde (MDA) levels were disrupted, indicating enhanced oxidative stress. Transcriptomic analysis of gills further revealed enrichment of ECM-receptor interaction, cell adhesion molecules, and leukocyte transendothelial migration pathways, suggesting that PS and MT may compromise immune function by interfering with extracellular matrix-related signaling, thereby exacerbating tissue damage and posing combined ecological risks in aquatic organisms.

This study aimed to investigate the effects of 17 alpha-Methyltestosterone (MT) on hepatic lipid metabolism in Gobiocypris rarus. G. rarus was exposed to varying concentrations of MT (0, 25, 50, and 100 ng/L) for durations of 7, 14, and 21 d. Biochemical and transcriptomic analyses were conducted using methods, such as ELISA, RTqPCR, Western Blotting, and RNA-seq, to decipher the key signals and molecular mechanisms triggered by MT in vivo. The results revealed that MT induced hepatomegaly in G. rarus and markedly increased the hepatic steatosis index (HSI). After 14 d of exposure, significant increase in PPAR gamma mRNA expression was observed, whereas after 21 d, PPAR alpha mRNA expression was significantly reduced. The expression pattern of SREBP1C mRNA initially decreased before increasing, mirroring the trend observed for SREBP1C protein expression. Furthermore, MT increased the levels of key lipid synthesis enzymes, including HSL, CPT1, GPAT, and FAS, thereby fostering lipid accumulation. RNA-seq analysis revealed that MT modulated hepatic bile acid metabolism via the PPAR pathway, consequently influencing cholesterol and lipid metabolism. Considering the differential metabolic pathways of MT across genders, it is postulated that MT may undergo aromatization to estrogen within G. rarus, thereby exerting estrogenic effects. These findings provide crucial experimental insights into the detrimental effects of MT in aquatic settings, underscoring its implications for safeguarding aquatic organisms and human health.

17α-Methyltestosterone (MT), an environmental endocrine-disrupting chemical (EDC), is widely present in aquatic environments, posing potential threats to the health of aquatic organisms. This study aimed to explore the protective effects of Vitamin C (VC) against MT-induced intestinal injury in Carassius auratus and evaluate the optimal VC dosage. C. auratus were exposed to 50 ng/L MT with 0, 25, 50, and 150 mg/kg VC for 7, 14, and 21 d. Intestinal pathological changes were assessed using paraffin sections, digestive enzyme activity was measured, RT-qPCR was used to analyze the expression of genes related to the intestinal barrier and inflammation, and 16S rDNA sequencing was conducted to evaluate the intestinal flora. MT exposure caused villus damage, vacuolization, and free lymphocytes. Additionally, it upregulated TNF-α and Claudin-12 expression and downregulated IL-10, Occludin, and Muc2 expression, exacerbating intestinal inflammation, damaging barrier function, and reducing digestive enzyme activity. VC at 25 and 50 mg/kg significantly alleviated MT-induced damage by restoring villus length and mitigating the downregulation of anti-inflammatory factors and tight junction protein-related genes while inhibiting TNF-α mRNA expression. 16S rDNA sequencing revealed that MT disrupted the intestinal flora and increased the abundance of harmful bacteria such as Acinetobacter, whereas VC promoted Lactobacillus production and enhanced digestive enzyme activity. We hypothesize that MT exposure promotes the growth of harmful bacteria in the intestines, leading to inflammation and damage to the mucosal barrier. 25 and 50 mg/kg VC can mitigate MT-induced intestinal injury by regulating the intestinal microbiota and have potential protective effects.

Polystyrene (PS) microplastics are pervasive environmental pollutants that are harmful to aquatic organisms upon degradation. The synthetic androgen 17α-methyltestosterone (MT) is an environmental endocrine-disrupting chemical. This study aimed to systematically evaluate the combined histological and molecular effects of MT and PS exposure on the liver and brain tissues of Danio rerio with focus on lipid metabolism and neural function disruption. Female D. rerio were exposed to 50 ng/L MT and 0.5 mg/L PS (5 μm in diameter) for 21 d. Histological observations, real-time quantitative PCR (qPCR), and RNA-sequencing (RNA-seq) analysis were employed to assess the effects of PS and MT. These results indicated that MT and PS co-exposure caused fatty degeneration of liver cells and a significant upregulation of lipid synthesis-related genes (ACSS1, CEL, FASN, and GK5). In brain tissue, the observed effects included reduced marginal layer neuron counts, cytoplasmic loosening of central layer neurons, disordered gray matter layer cells, and vascular congestion. RNA-seq analysis further revealed significant enrichment of differentially expressed genes in the “glycine, serine, and threonine metabolism” and “neuroactive ligand-receptor interaction” signaling pathways. Thus, MT and PS co-exposure induced lipid metabolism disorders in D. rerio and influence neural signaling by altering the “neuroactive ligand-receptor interaction” pathway. These findings highlight the complex risks posed by environmental pollutants to aquatic life and provide critical insights for environmental protection and aquatic health research.

Poly(I:C) and lipopolysaccharide (LPS), two well-known pathogen-associated molecular patterns of viruses and bacteria, respectively, are frequently utilized to study host immunological responses to infections. Analysis of the gene expression profile in the spleen of Ussuri catfish (Pseudobagrus ussuriensis) infected with poly(I:C) or LPS at 0, 3, 12, and 24 h was the goal of the current study. After infection with LPS, each comparison group shared 34 differentially expressed genes (DEGs), but after infection with poly(I:C), 816 DEGs were shared. Following LPS or poly(I:C) infection, 10 DEGs were expressed differently in each group. The ECM-receptor interaction route and the cytokine-cytokine receptor interaction pathway were found to be the most enriched pathways for DEGs across all groups. B-type lectin, Protein FAM110B, CDK17, Lumican, Netrin-4, and nuclear receptor subfamily 4 group A member 2 (NR4A2) all showed significant variations in their expression levels. Potential expression patterns found in the study might be helpful diagnostic tools for monitoring Ussuri catfish illness.

Globally, approximately 80 % of wastewater is discharged into aquatic environments without proper treatment, introducing hazardous compounds into ecosystems. Pollutant interactions can cause synergistic toxicity in aquatic organisms; however, their combined effects remain poorly understood. Zebrafish (Danio rerio H.) were exposed to polystyrene (PS) microplastics and 17α-methyltestosterone (MT) for 21 d, followed by pathological analysis, enzyme activity assays, and quantitative real-time PCR to assess metabolism- and immunity-related gene expression. Integrated transcriptomic and metabolomic analyses were conducted to elucidate the molecular mechanisms of PS- and MT-induced toxicity in the liver and brain. In the liver tissue, dysregulation of lipid metabolism genes (CYP1A/3A, PPARα, and SREBP-1) led to excessive lipid accumulation and hepatic steatosis. In brain tissue, reduced glutathione peroxidase activity, coupled with elevated glutathione reductase and cytochrome P450 activities, exacerbated oxidative stress, compromising neuronal integrity. Exposure to PS and MT significantly upregulated inflammatory genes (TNF-α and IL-1β) and downregulated oxidative stress-related genes (GPx4b, Nrf2, and HO-1) in both tissues, intensifying oxidative damage and inflammatory responses. Combined analysis of liver metabolomics and brain transcriptomics revealed that PS and MT exposure significantly disrupted sphingolipid metabolism. Hepatic metabolic disorders may affect brain function via the liver-brain axis by activating neuroactive ligand-receptor interaction and calcium signaling pathways, thereby disrupting neurotransmitter homeostasis and causing neuronal damage.

In recent years, the use of endocrine-disrupting chemicals (EDCs) has become increasingly common, leading to severe environmental pollution and harm to aquatic organisms. 17α-Methyltestosterone (MT) is a synthetic androgen that can cause immunotoxicity in aquaculture, affecting fish health. To address this issue, this study aimed to investigate the effect of Vitamin C (VC) on MT-induced immunotoxicity and determine the optimal VC supplementation. Carassius auratus was exposed to 50 ng/L MT and treated with 25, 50, and 150 mg/kg VC for 7, 14, and 21 d. Morphological indicators, histological characteristics, hepatic antioxidant capacity, and immune-related gene expression were analyzed. Additionally, RNA-seq was performed on the liver tissues of the control, MT, and MT + 25 mg/kg VC groups after 21 d. Results showed that, MT treatment significantly increased liver malondialdehyde content and inhibited immune-related gene expression (TNF-α, IL-8, INF-γ, IL-10, Caspase-9, and IGF-I), causing oxidative stress and immunotoxicity, leading to hepatic steatosis. However, supplementation with 25–50 mg/kg VC effectively alleviated the MT-induced damage to the hepatic structure and immune system. RNA-seq revealed significant enrichment of differentially expressed genes in multiple signaling pathways, including the mTOR, MAPK, and Wnt pathways. In summary, 25–50 mg/kg VC alleviated inhibitory effect of MT on immune-related genes in C. auratus liver, reducing MT-induced tissue damage. VC not only alleviated inflammation, oxidative stress, and immunotoxicity induced by MT through the regulation of the mTOR, MAPK, and Wnt signaling pathways, but also indirectly enhanced cellular antioxidant defense mechanisms by regulating the NRF2 pathway. This provides a theoretical basis for VC application in aquaculture, improving fish health and increasing efficiency.

Polystyrene microplastics (PS-MPs) are important carriers of pollutants in water. 17 alpha-Methyltestosterone (MT) is a synthetic environmental endocrine disrupting chemical (EDC) with androgenic effects. To study the effects of PS-MPs and MT on zebrafish reproductive systems, zebrafish were exposed to 0 or 50 ng L-1 MT, 0.5 mg center dot L-1 PS-MPs, or 50 ng center dot L-1 MT + 0.5 mg center dot L-1 PS-MPs for 21 d. The results showed that the different exposure reagents caused varying degrees of damage to the reproductive systems in zebrafish, with the extent of damage increasing as the exposure duration increased. Histological analysis of the gonads revealed that the ratio of mature oocytes and mature spermatozoa in the gonad decreased gradually with increased exposure time, with the ratio being Control > PS-MPs > MT > MT + PS-MPs in decreasing order. The results of quantitative real-time PCR (qRT-PCR) showed that in female fish treated for 7 d, the expression of cyp11a mRNA was significantly reduced in all three treatment groups(MT, PS-MPs, and MT + PS-MPs), while in the group treated for 14 d with MT + PS-MPs, the expression of cyp19a1a and StAR mRNA was significantly increased. In male fish exposed for 21 d, the expression of cyp11a, cyp17a1, cyp19a1a, StAR, 3 beta-HSD, and 17 beta-HSD3 mRNA was significantly decreased in MT + PS-MPs. ELISA results showed that after 14 d of exposure, the levels of E2, LH, and FSH in the ovaries of female fish were significantly reduced in all three treatment groups. Similarly, the levels of T, E2, LH, and FSH in the testis of male fish were significantly reduced after 14 d of exposure to PS-MPs and MT + PS-MPs. Offspring of zebrafish exposed to MT and MT + PS-MPs exhibited delayed incubation time and slow development. The cross-generational toxicity of PS-MPs themselves may be negligible, but it can exacerbate the toxicity of MT, making the cross-generational effects more pronounced in the offspring, causing offspring mortality and malformations. Offspring of zebrafish exposed to MT and MT + PS-MPs exhibited delayed incubation time and slow development. In addition, MT caused malformations such as pericardial edema, yolk cysts, and spinal deformities in zebrafish during the incubation period.

Fishes are susceptible to hypoxia stress, while the common carp is known for its high tolerance to hypoxia. The hypoxia-inducible factor (HIF) pathway directly regulates the cell’s response to hypoxia. Still, it is currently unknown which members of the hif-α genes are present in common carp and their specific functions. In this study, we found that the hif-1α, hif-2α, and hif-3α genes of common carp all contained twice the number of copies of their orthologs in zebrafish. Common carp has four copies of the hif-1α gene, of which the two hif-1αa genes were expressed at low levels in the vast majority of tissues, while the two hif-1αb genes were expressed at high levels in multiple tissues. We silenced the two hif-1αb genes using chitosan nanoparticles (CSNPs) carrying siRNA and subjected two groups to hypoxic stress. Transcriptome sequencing results show that whether under normoxia or hypoxia, the number of differentially expressed genes (DEGs) caused by silencing the hif-1αb genes in the heart exceeds 1,000, far more than the number of DEGs in the gills or brain. GO enrichment and KEGG enrichment showed that DEGs in the heart were mainly related to immune function and myocardial contraction. DEGs in the gills and brain also enriched many immune-related terms, and some DEGs in the gills were related to iron metabolism and erythropoiesis. Among the paralogs, the two hif-1αa genes were most obviously up-regulated under normoxia, while the hif-3α genes were most obviously up-regulated under hypoxia. We did not find any downstream genes of the HIF pathway that were specifically regulated by the hif-1αb genes. The main effect site of the common carp hif-1αb genes is the heart, and their main functions are to regulate immune response and myocardial contraction. Their functions are partially redundant with the hif-1αa genes and hif-3α genes. When their expressions are inhibited, the expression of hif-1αa genes or hif-3α genes would be up-regulated in specific contexts, thereby compensating for their loss of function. The downstream genes of the HIF pathway in common carp may be generally regulated by multiple hif-α genes.

Pseudobagrus ussuriensis is an unscaled fish that is more susceptible to skin damage than scaled fish. To investigate the impacts of hypoxia and reoxygenation on skin and brain immunity, juvenile P. ussuriensis were subjected to hypoxia conditions (DO: 0.8 ± 0.05 mg/L) for durations of 0, 3, 6, and 12 h, followed by 12 h of reoxygenation (DO > 6 mg/L). Histological analysis showed a significant increase in the number of skin mucosal cells after 12 h of hypoxia and a significant decrease after 12 h of reoxygenation when compared to the control group. As the duration of hypoxia increased, an increase in antioxidant (SOD, CAT, GSH, MDA) and immune (cortisol, LZM) physiological parameters of the skin and brain appeared. The results of transcriptomic studies showed that the number of differential genes was greater in skin than in brain. Most of the immune pathways in both tissues under hypoxia conditions were all nonspecific immunity (TNF, IL-17, chemokines), while both tissues maintained their homeostasis through active energy supply and cell cycle regulation. Meanwhile, both physiological parameters and RNA transcriptome results showed that 12 h of reoxygenation could not completely eliminate the negative effects of 12 h of hypoxia. This study offers new insights into the immune responses of P. ussuriensis skin and brain during acute hypoxia and reoxygenation.

17α-Methyltestosterone (MT), a synthetic environmental endocrine disruptor with androgenic effects, has been shown to disrupt the reproductive system and inhibit germ cell maturation in Gobiocypris rarus. To further investigate the regulation of gonadal development by MT through the hypothalamic-pituitary-gonadal (HPG) axis, G. rarus were exposed to 0, 25, 50, and 100 ng/L of MT for 7, 14, and 21 days. We analyzed its biological indicators, gonadotropin-releasing hormone (GnRH), gonadotropins, reproduction-related gene expression, and brain tissue transcriptome profiles. We found a significant decrease in the gonadosomatic index (GSI) in G. rarus males exposed to MT for 21 days compared to the control group. GnRH, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) levels, as well as the expressions of the gnrh3, gnrhr1, gnrhr3, fshβ, and cyp19a1b genes, were significantly reduced in the brains of both male and female fish when exposed to 100 ng/L MT for 14 days compared to the controls. Therefore, we further constructed four RNA-seq libraries from 100 ng/L MT-treated groups of male and female fish, obtaining 2412 and 2509 DEGs in male and female brain tissue, respectively. Three common pathways were observed to be affected in both sexes after exposure to MT, namely, nicotinate and nicotinamide metabolism, focal adhesion, and cell adhesion molecules. Furthermore, we found that MT affected the PI3K/Akt/FoxO3a signaling pathway through the upregulation of foxo3 and ccnd2, and the downregulation of pik3c3 and ccnd1. Therefore, we hypothesize that MT interferes with the levels of gonadotropin-releasing hormone (GnRH, FSH, and LH) in G. rarus brains through the PI3K/Akt/FoxO3a signaling pathway, and affects the expression of key genes in the hormone production pathway (gnrh3, gnrhr1 and cyp19a1b) to interfere with the stability of the HPG axis, thus leading to abnormal gonadal development. This study provides a multidimensional perspective on the damaging effects of MT on fish and confirms that G. rarus is a suitable model animal for aquatic toxicology.

目的 旨在探讨把握老人跌倒现状,探究居家养老老人跌倒的影响因素,以提升老年人的健康水平,减轻由于跌倒所造成的疾病经济负担,对实现健康老龄化具有重要意义.方法 基于中国老年健康影响因素跟踪调查(CLHLS)2018年数据,归纳居家养老老人跌倒现状,采用卡方、logistic回归分析影响居家老人跌倒的主要因素.结果 结果显示9867名老人年跌倒发生率(人)为23.5％;年跌倒发生(次)率为41.3％.多因素结果显示屋内有霉味(OR=1.209,95％ CI:1.044～1.400)、屋内存在漏雨漏水情况(OR=1.499,95％ CI:1.371～1.707)、经常锻炼身体(OR=1.224,95％ CI:1.092～1.371)、听力差(OR=1.275,95％CI:1.140～1.427)是居家老人跌倒的危险因素;低龄(OR=0.631,95％CI:0.058～0.784)、无慢性病(OR=0.650,95％CI:0.056～0.747)、维持独立站立(OR=0.659,95％ CI:0.584～0.744)、清淡饮食习惯(OR=0.871,95％CI:0.785～0.965)是居家老人跌倒的保护因素.结论 我国居家养老老人年跌倒发生率较高,应通过改善潮湿居住环境、控制饮食等措施来预防痛风、糖尿病足等脚部疾病的发生.老人应该通过适当、多维度的身体运动来改善肌肉力量,维持关节灵活性以保持身体的动态平衡能力,从而增强独立站立能力,尽可能延长站立时间,降低跌倒的风险.

目的:探寻我国卫生资源脆弱性地区和导致脆弱性存在的关键性障碍因子,为降低我国卫生资源系统脆弱性提供决策参考依据.方法:利用熵权法确定评价指标权重,利用均值标准差法、秩和法对31个省份脆弱性等级及关键障碍性因子进行评价.结果:17个指标熵权基尼系数为0.52.卫生资源极度脆弱的省份为西藏和新疆.极为关键障碍因子是人均可支配收入、城镇化水平和婴儿死亡率3个指标.结论:我国卫生资源系统综合脆弱性是一种社会因素决定为主的压力主导型的,在空间分布上呈现一种"海拔效应",破解我国卫生资源系统脆弱性的核心在于促进和提高经济和社会发展水平.

目的 了解影响我国独居老人自评健康状况的影响因素,为改善我国独居老人健康及生活质量提供参考依据.方法 通过自评问卷调查方法,采用2018年中国老年健康影响因素跟踪调查(CLHLS)数据,了解独居老人健康状况,采用卡方检验以及多因素logistic回归方法分析独居老人健康状况的影响因素.结果 1236名独居老年人中,自评健康较好的有551人,占比44.6％,较差的685人,占比55.4％;子女经常看望(OR =1.840,95％CI:1.080～3.135)、体育锻炼(OR=1.813,95％CI:1.385 ～2.372)、饮酒(OR=1.531,95％CI:1.061～2.209)、体检(OR =1.347,95％ CI:1.033 ～1.756)、慢性病(OR =0.682,95％ CI:0.532～0.875)、霉味(OR =0.533,95％CI:0.391～0.726)、睡眠6～9小时(OR =0.528,95％ CI:0.393 ～0.710)、睡眠时间＞9小时(OR =0.411,95％ CI:0.283～0.597)与独居老人自评健康有关.结论 我国独居老人自评健康状况总体较差.应重视独居老人的子女关怀、生活行为方式、居住环境及慢性病状况等,更好地改善独居老人的健康状况.

目的 探求我国老年人的生活满意度及其影响因素,为有关部门制定提高老年人生活质量的有效措施提供建议和理论依据.方法 基于中国老年健康影响因素跟踪调查(CLHLS)2018年的数据,运用卡方检验和Logistic回归方法分析我国老年人生活满意度及其影响因素.结果 影响老年人生活满意度的因素为老年人的活动能力(OR=1.683,95％CI:0.533～0.662)、受教育程度(OR=1.221,95％CI:1.100～1.355)、经济水平(OR=6.667,95％CI:0.118～0.190)、生活来源(OR=1.741,95％CI:1.498～2.024)、及时到达医院(OR=1.753,95％CI:1.336～2.301)、进行常规体检(OR=1.311,95％CI:1.172～1.465)、以及社区支持(OR=1.283,95％CI:1.154～1.425,P＜0.001).结论64.7％的老年人对目前的生活比较满意,应该引导老年人改善自身健康水平,提升老年人的受教育程度和文化素养,提高老年人的经济水平,完善社会保障制度,合理配置医疗服务,提高卫生服务的可及性、加强社区支持与人文关怀,提升老年人的生活质量.