Fast-growing broilers are prone to pulmonary hypertension, which is the main cause of death in broilers with ascites syndrome (AS). The underlying mechanisms of AS and the role of metabolomics changes involved in this pathological process are still not fully understood. In this study, 180 1-day-old Arbor Acres broilers were randomly divided into the test group (injected intravenously with carboxymethyl cellulose CM-32 ion exchange suspension) and the control group (injected with the same volume of saline). A comprehensive metabolic analysis based on liquid chromatography-tandem mass spectrometry (LC-MS/MS) on the sera of the test group and the control group was conducted to identify the metabolomics profiles. Results showed significant differences in packed cell volume (PCV), hemoglobin in blood (HGB), right ventricle wall/total ventricle (RV/TV) value, and body weight between the test group and control group. Significant variations in the levels of 29 metabolites were found between the two groups, among which 17 metabolites showed a remarkable increase and 12 metabolites significantly reduced. Metabolomics analysis showed that major alterations were related to purine metabolism, glycerol phospholipid metabolism, phenylalanine metabolism and biosynthesis of phenylalanine, tyrosine and tryptophan. The study uncovered AS pathogenesis in broilers, offering new insights for diagnostic and therapeutic targets.

Mn2O3 nanometer particles(Mn2O3 NPs), a new material, is widely used in medicine, electrochemical sensing and energy storage fields. The widespread use of Mn2O3 NPs has caused health concerns, and it is necessary to clarify the toxic mechanism of Mn2O3 NPs exposure. Our findings showed that Mn2O3 NPs exposure could lead to liver histological abnormalities, mitochondrial dysfunction in liver, as well as mitochondrial-mediated apoptosis, autophagy and mitochondrial dynamics disorder, and eventually lead to liver injury. At the same time, the ileal epithelium suffered physiological damage and inflammation after Mn2O3 NPs exposure, and the expression levels of genes and proteins related to intestinal barrier function (MUC1 ZO-1 Claudin1 and Occludin) were significantly down-regulated. Meanwhile, 16s sequencing analysis of intestinal bacteria showed that Mn2O3 NPs exposure caused significant changes in intestinal flora abundance. The Firmicutes/Bacteroidetes ratio increased, and the abundance of probiotics (Bacteroides, Bifidobacterium, Faecalibacterium) decreased, while the abundance of harmful bacteria (Streptococcus, Enterococcus, Pseudomonas) increased. The changes in these microflorae may potentially impact the development of liver injury. Altogether, these results provide novel insights into the potential mechanism of Mn2O3 NPs related hepatotoxicity induced by gut microbiota via the gut-liver axis, and contribute to a better interpretation of the health impact of Mn2O3 NPs.

Pulmonary hypertension syndrome (PHS), a metabolic disorder causing economic losses in broilers, arises from hypoxia-induced portal hypertension and liver cirrhosis, triggering mitochondrial oxidative damage, excessive ROS production, and altered mitochondrial biogenesis. This study explored terpinen-4-ol (T4O), known for antimicrobial and anti-inflammatory properties, in mitigating PHS. Broilers were divided into four groups, including PHS-affected birds with/without T4O supplementation. Analyses revealed that PHS birds exhibited reduced antioxidant capacity, elevated MDA and ROS levels, increased mitochondrial numbers, and upregulated expression of oxidative stress markers (Keap1, HO-1, Nrf-2) and mitochondrial biogenesis regulators (PGC-1α, Nrf-1, Tfam). T4O administration enhanced antioxidant activity, reduced ROS and MDA, suppressed compensatory mitochondrial proliferation, and downregulated Keap1/Nrf-2 and mitochondrial biogenesis pathways. These effects suggest that T4O alleviates hypoxia-driven oxidative stress and mitochondrial dysfunction in broilers. Findings highlight T4O’s potential as a therapeutic agent to mitigate PHS-related losses in poultry production.

Aflatoxin B1 (AFB1) is the most prevalent and toxic class of aflatoxins, which is considered a significant risk factor for food safety. Curcumin, a phytoconstituent with anti-inflammatory and antioxidant properties, has potential therapeutic value for intestinal inflammatory diseases. In this study, the duckling model susceptible to AFB1 was selected for toxicity testing, aiming to explore the effect of curcumin on AFB1 enterotoxicity and its possible mechanism of action. The results showed that curcumin promoted the growth and development of ducklings and mitigated the changes in morphology and permeability serological index (DAO and D-LA) after AFB1 exposure. Curcumin also mitigated AFB1-induced oxidative stress by activating the Nrf2 pathway, and ameliorated intestinal inflammation by inhibiting the NF-κB/IκB signaling pathway and boosting intestinal autophagy. In terms of gut flora and their metabolites, we found that curcumin supplementation significantly increased the intestinal flora's abundance index and diversity index compared to the AFB1 group, mitigating the decline in the abundance of Actinobacteria and the rise in that of harmful bacteria Clostridia. Furthermore, untargeted metabolomic analysis revealed that the protective effect of curcumin on the intestine was mainly through the regulation of AFB1-induced disorders of lipid metabolism, involving linoleic acid metabolism, α-linolenic acid metabolism, and glycerolipid metabolism. Overall, the enteroprotective effects of curcumin may be of significant value in the future for treating chronic AFB1 poisoning and also provide new therapeutic ideas for other mycotoxicosis.

PURPOSE:While copper (Cu) is essential for biological organisms, excessive Cu can be harmful. Ferroptosis is a programmed cell death pathway, but the role of ferroptosis in renal injury induced by Cu is limited. The aim of this study was to investigate the role of ferroptosis in kidney injury in chickens and the molecular mechanism by which Cu promotes renal ferroptosis. MATERIALS AND METHODS:Chicken were subjected to Cu treatment by artificially adding excess Cu to the basal diet (the Cu concentration in the diet was supplemented to 110-330 mg/kg), and the impact on kidney fibrosis, tissue structure, and ferroptosis-related molecular markers was studied. Then, the expression levels of genes and proteins related to ferroptosis, iron metabolism and ferroautophagy were detected to explore the promoting effect of Cu on ferroptosis in chicken kidney. MAIN FINDINGS:Cu treatment resulted in significant fibrosis and tissue structure damage in chicken kidneys. Molecular analysis revealed a significant upregulation of LC3Ⅱ, P62, ATG5, and NCOA4, along with a decrease in FTH1 and FTL protein levels. Additionally, crucial markers of ferroptosis, including the loss of GPX4, SLC7A11, and FSP1, and an increase in PTGS2 and ACSL4 protein levels, were observed in chicken kidneys after Cu exposure. CONCLUSION:Our study showed that dietary Cu excess caused kidney injury in brochickens and exhibited ferroptosis-related features, including lipid peroxidation, reduction of ferritin, and downregulation of FSP1 and GPX4. These results indicate that excess Cu can induce renal ferroptosis and lead to kidney injury in chickens. This study highlights the complex interplay between Cu ions and ferroptosis in the context of renal injury and provides a new perspective for understanding the mechanism of Cu-induced renal injury.

This study explores the status and lessons learned from veterinary medicine and its One health perspective in academia, comparing the systems of China with the rest of the world. For this purpose, multiple databases, including PubMed, CNKI, Web of Science, etc., were used to analyze various aspects of veterinary education in China. The paper is structured into sections including veterinary medicine in academic institutions, the development of veterinary culture, the status of veterinary education in China, issues and challenges, international comparisons, and optimization suggestions. In this study, a simple approach to the historical evolution of veterinary education in different developmental stages is revealed through a retrospective analysis. The section on the status of veterinary education in China focuses on critical areas such as talent cultivation, practical teaching and internships, educational evaluation systems, professional education, and innovation and entrepreneurship. Through the analysis of challenges and issues in Chinese veterinary education, the paper reveals inadequacies in curriculum systems and imbalances in internship and practical opportunities. Comparing with Europe, America, and developing countries, this paper offers insights and inspirations to guide the 'future development of veterinary education in China. Finally, the paper proposes optimization suggestions, including improvements to the curriculum system, strengthening practical teaching, and promoting international cooperation and exchange. These measures aim to propel Chinese veterinary education towards a healthier, more diverse, and internationalized direction, enhancing the overall quality of veterinary professionals to meet better veterinary workers, nonhuman animals, and one health in societal development.

1. The following study investigated the relationship between pulmonary hypertension syndrome (PHS) and mitochondrial dynamics in broiler cardiomyocytes.2. An animal model for PHS was established by injecting broiler chickens with CM-32 cellulose particles. Broiler myocardial cells were cultured under hypoxic conditions to establish an in vitro model. The ascites heart index, histomorphology, mitochondrial ultrastructure, and mitochondrial dynamic-related gene and protein expression were evaluated.3. The myocardial fibres from PHS broilers had wider spaces and were wavy and twisted and the number of mitochondria increased. Compared with the control group, the gene and protein expression levels were decreased for Opa1, Mfn1, and Mfn2 in the myocardium of PHS broilers. The gene and protein expression was significantly increased for Drp1 and Mff.4. This study showed that PHS in broilers may cause myocardial mitochondrial dysfunction, specifically by diminishing mitochondrial fusion and enhancing fission, causing disturbances in the mitochondrial dynamics of the heart.

As an efficient alternative copper (Cu) source, copper nanoparticles (nano-Cu) have been widely supplemented into animal-producing food. Therefore, it is necessary to assess the effect of nano-Cu exposure on the biological health risk. Recently, the toxic effects of nano-Cu have been confirmed but the underlying mechanism remains unclear. This study reveals the impact of nano-Cu on endoplasmic reticulum autophagy (ER-phagy) in chicken hepatocytes and further identifies Drp1 and its downstream gene FAM134B as crucial regulators of nano-Cu-induced hepatotoxicity. Nano-Cu exposure can induce Cu ion overaccumulation and pathological injury in the liver, trigger excessive mitochondrial fission and mitochondria-associated membrane (MAM) integrity damage, and activate ER-phagy in vivo and in vitro. Interestingly, the knockdown of Drp1 markedly decreases the expression of FAM134B induced by nano-Cu. Furthermore, the expression levels of ATL3, CCPG1, SEC62, TEX264, and LC3II/LC3I induced by nano-Cu exposure are decreased by inhibiting the expression of Drp1. Simultaneously, the inhibition of FAM134B effectively alleviates nano-Cu-induced ER-phagy by downregulating the expression of ATL3, CCPG1, SEC62, TEX264, and LC3II/LC3I. Overall, these results suggest that Drp1-mediated impairment of MAM integrity leads to ER-phagy as a novel molecular mechanism involved in the regulation of nano-Cu-induced hepatotoxicity. These findings provide new ideas for future research on the mechanism of nano-Cu-induced hepatotoxicity.

With the application of copper nanoparticles (nano-Cu) in livestock and poultry feed addition, their biotoxicity has been gradually recognized. Therefore, it has become an urgent problem to find the effective natural antagonists to reduce the toxicity of copper nanoparticles. Here, we found that hesperidin could alleviate nano-Cu-induced pathological injury in the immune organs of chickens via the histopathological examination of the spleen, thymus, and bursa of Fabricius. Additionally, the results of western blot showed that nano-Cu exposure activated ZBP1-mediated PANoptosis in immune organs, with evidenced by the significant up-regulation of ZBP1 signal molecule and PANoptosis-related proteins (apoptosis: Caspase-7, Caspase-3, Caspase-8; pyroptosis: Caspase-1, GSDMD, GSDME; necroptosis: RIPK1 and MLKL). Besides that, immunohistochemistry and immunofluorescence also showed that the staining intensity of Caspase-9 and Caspase-8 proteins was observably elevated in nano-Cu group compared to control group, and the staining intensity of the hesperidin mixed nano-copper group was markedly lower than that of the nano-Cu group. Meanwhile, hesperidin effectively attenuated the ZBP1 expression and PANoptosis under nano-Cu exposure. These findings suggested that excessive nano-Cu could cause ZBP1-drived PANoptosis in immune organs, while hesperidin could alleviate toxic damage induced by nano-Cu exposure.

Abstract As a pesticide, thiram is widely used in agriculture to eliminate pests, and it also causes great environmental pollution and poses a certain threat to animal health. It’s well known that the contamination of feed with thiram in the environment can lead to tibial chondrogenesis(TD) in chickens. The imbalance of intestinal flora and related metabolites is closely related to bone development. Unfortunately, the relationship between the intestinal flora of TD broilers and serum metabolites is unclear. Our results demonstrated that broilers exposed to thiram showed typical lameness and the white cartilage thrombus in the growth plate, accompanied by hepatotoxicity and intestinal injury. We found that the intestinal flora of TD group was out of balance, the diversity was significantly increased with Corynebacterium significantly enriched. Moreover, the metabolome results showed alterations in 10 serum metabolites, with Glucosylceramide being considerably up-regulated, resulting in sphingolipid metabolism problem, which is critical in the etiology of TD. The comprehensive correlation analysis showed the relationship between intestinal microflora and Sphingolipid metabolism in TD broilers. Thiram aggravates tibial chondrodysplasia by affecting the changes in the composition and structure of the intestinal microflora of broilers and the disorder of sphingomyelin metabolism. Collectively, these findings provide novel insight into the pathogenesis of TD from the perspective of thiram-induced gut microbiota and metabolic disorders.

兽医学教育是培养应用型的兽医人才,学生不仅要有扎实的专业理论基础,娴熟的操作技能,更重要的是能够将这些知识和技能转化为执业兽医能力.《兽医临床病理学实验课》的课程是以掌握兽医临床病理样本的临床检验技术为核心,培养学生拥有临床检验与诊疗能力的学科.

Copper (Cu) is pollution metal that is a global concern due to its toxic effects. A recent study found that the release of mitochondrial DNA (mtDNA) into the cytoplasm can activate the innate immune response, but the exact mechanisms underlying the effect of Cu exposure remains unknown. In this study, we identified that the reduction in transcription Factor A (TFAM) led to mtDNA leakage into the cytoplasm under Cu exposure in hepatocytes, accompanied by the activation of the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway-mediated innate immunity (increased expression of cGAS, STING, TANK-binding kinase-1 (TBK1), and interferon regulatory factor-3 (IRF3)) genes and proteins, and enhanced phosphorylation levels of TBK1 and IRF3). Subsequently, silencing TFAM (siTFAM) significantly aggravated mtDNA release and the innate immune response under Cu treatment. Mitochondrial DNA depletion alleviated Cu-induced innate immunity in hepatocytes, while mtDNA transfection further enhanced the innate immune response. Notably, the inhibition of STING effectively alleviated the phosphorylation levels of the TBK1 and IRF3 proteins induced by Cu, while the upregulation of STING aggravated the Cu-induced innate immunity. Furthermore, EtBr and H-151(a STING inhibitor) treatment dramatically reversed the effect of TFAM depletion on the sharpened innate immune response induced by Cu via the cGAS-STING pathway. In general, these findings demonstrated the TFAM deficiency promotes innate immunity by activating the mtDNA-cGAS-STING signalling pathway under Cu exposure in hepatocytes, providing new insight into Cu toxicology.

Copper (Cu) is a toxic heavy metal pollutant. The hepatic toxicity of Cu has attracted widespread attention from researchers. However, its underlying mechanism remains elusive. Mitochondrial microRNAs (mitomiRs) are considered important factors in regulating mitochondrial and cellular functions, and their roles have been implicated in the mechanisms of metal toxicity. Therefore, this research revealed the changes in the mitomiRs expression profile of chicken liver after Cu exposure. It was ultimately determined that mitomiR-1736-3p can be involved in Cu-induced chicken liver damage by targeting AATF. In particular, our investigations have uncovered that exposure to Cu can trigger heightened levels of apoptosis in the hepatic tissue of chickens and primary chicken embryo hepatocytes (CEHs). It is noteworthy that we found upregulation of miR-1736-3p expression can exacerbate Cu-induced cell apoptosis, while inhibition of miR-1736-3p can effectively reduce apoptosis occurrence. Subsequently, we found that Cu-induced cell apoptosis could be restored by overexpressing AATF, while silencing AATF exacerbated the level of apoptosis. Fascinatingly, this change in apoptotic level is directly influenced by AATF on Bax and Bak1, rather than on p53 and Bcl-2. Overall, these findings suggest that the mitomiR-1736-3p/AATF axis mediates the mitochondrial pathway of cell apoptosis potentially involved in Cu-induced chicken liver toxicity.

Thiram is a plant fungicide, its excessive use has exceeded the required environmental standards. It causes tibial dyschondroplasia (TD) in broilers which is a common metabolic disease that affects the growth plate of tibia bone. It has been studied that many microRNAs (miRNAs) are involved in the differentiation of chondrocytes however, their specific roles and mechanisms have not been fully investigated. The selected features of tibial chondrocytes of broilers were studied in this experiment which included the expression of miR-181b-1-3p and the genes related to WIF1/Wnt/β-catenin pathway in chondrocytes through qRT-PCR, western blot and immunofluorescence. The correlation between miR-181b-1-3p and WIF1 was determined by dual luciferase reporter gene assay whereas, the role of miR-181b-1-3p and WIF1/Wnt/β-catenin in chondrocyte differentiation was determined by mimics and inhibitor transfection experiments. Results revealed that thiram exposure resulted in decreased expression of miR-181b-1-3p and increased expression of WIF1 in chondrocytes. A negative correlation was also observed between miR-181b-1-3p and WIF1. After overexpression of miR-181b-1-3p, the expression of ACAN, β-catenin and Col2a1 increased but the expression of GSK-3β decreased. It was observed that inhibition of WIF1 increased the expression of ALP, β-catenin, Col2a1 and ACAN but decreased the expression of GSK-3β. It is concluded that miR-181b-1-3p can reverse the inhibitory effect of thiram on cartilage proliferation and differentiation by inhibiting WIF1 expression and activating Wnt/β-catenin signaling pathway. This study provides a new molecular target for the early diagnosis and possible treatment of TD in broilers.

Pulmonary hypertension syndrome (PHS) is a poultry disease that causes significant economic losses in broilers. Portal hypertension and liver cirrhosis can cause ascites formation. Disturbance of mitochondrial dynamics causes several diseases; however, its mechanism of action in PHS is not yet fully understood. In this research, 210 broilers were split randomly into two groups: control and PHS. Broilers in the control group were injected with normal saline and those in the PHS group were injected with CM-32 cellulose particles at 20 days of age. Transmission electron microscopy (TEM) was used to assess mitochondrial ultrastructure. Changes in mitochondrial dynamics were measured by immunohistochemical staining, RT-PCR and western blotting. On days 28 and 42, the liver and heart were collected from each group, and the ascites heart index (AHI) and hepatic coefficient were calculated. The results showed that PHS induced hepatocyte damage, reduced mitochondrial size, and increased mitochondrial number. Furthermore, RT-PCR demonstrated the downregulation of Mfn1, Mfn2, and Opa1 mRNA, and the upregulation of Drp1 and Mff mRNA. Protein expression levels detected by immunohistochemistry and western blotting were similar to those obtained by RTPCR. This study showed that mitochondrial fusion in the liver was diminished and mitochondrial fission in the liver was enhanced in PHS broilers.

Copper (Cu) is hazardous metal contaminant, which induced hepatotoxicity is closely related to mitochondrial disorder, but exact regulatory mechanism has not yet been revealed. Mitochondrial microRNAs (mitomiRs) are a novel and critical regulator of mitochondrial function and mitochondrial homeostasis. Hence, this study revealed the impact of Cu-exposure on mitomiR expression profiles in chicken livers, and further identified mitomiR12294-5p and its target gene CISD1 as core regulators involved in Cu-induced hepatotoxicity. Additionally, our results showed that Cu-exposure induced mitochondrial oxidative damage, and mitochondrial quality control imbalance mediated by mitochondrial dynamics disturbances, mitochondrial biogenesis inhibition and abnormal mitophagy flux in chicken livers and primary chicken embryo hepatocytes (CEHs). Meaningfully, we discovered that inhibition of the expression of mitomiR-12294-5p effectively alleviated Cu-induced mitochondrial oxidative stress and mitochondrial quality control imbalance, while the up-regulation of mitomiR-12294-5p expression exacerbated Cu-induced mitochondrial damage. Simultaneously, the above Cu-induced mitochondrial damage can be effectively rescued by the overexpression of CISD1, while knockdown of CISD1 dramatically reverses the mitigating effect that inhibition of mitomiR-12294-5p expression on Cu-induced mitochondrial oxidative stress and mitochondrial quality control imbalance. Overall, these results suggested that mitomiR-12294-5p/CISD1 axis mediated mitochondrial damage is a novel molecular mechanism involved in regulating Cu-induced hepatotoxicity in chickens.

Tibial dyschondroplasia (TD) is a metabolic bone disease that occurs in fast-growing chickens and can lead to substantial economic damages and compromise the poultry welfare. Triptolide is a traditional Chinese medicine (TCM), which has been broadly used as an anti-inflammatory, and anti-cancerous drug. However, its therapeutic role against tibial dyschondroplasia is under-reported yet. Therefore, the study aimed for investigating the protective effect of triptolide against autophagy and apoptosis in TD affected chickens. Random classification of chickens (n=30) was done into three groups: CON, TD and triptolide treatment group (TP). All chickens were given standard diet until the end of the experiment for 18 days. In this study, tibial bone was collected for analyzing several aspects, serum was collected for biochemical analysis, and microscopic assessment was done by H&E staining. Immunohistochemistry, immunofluorescence, western blotting, and RT-qPCR were used to detect autophagy and apoptosis-related proteins and genes. Observations illustrated that after triptolide treatment, the symptoms of TD group were improved, and tibial parameters were changed. At the same time, the expression of m-TOR and P62 mRNA in TP group showed significant decrease comparing to TD group. Precisely, thiram induced TD was found to be involved in hypertrophic chondrocytes apoptosis and autophagy, and triptolide showed protective effects against TD.

Copper (Cu) is an essential trace element that plays a crucial role in numerous physiopathological processes related to human and animal health. In the poultry industry, Cu is used to promote growth as a feed supplement, but excessive use can lead to toxicity on animals. Cytochrome P450 enzymes (CYP450s) are a superfamily of proteins that require heme as a cofactor and are essential for the metabolism of xenobiotic compounds. The purpose of this study was to explore the influence of exposure to Cu on CYP450s activity and apoptosis in the jejunum of broilers. Hence, we first simulated the Cu exposure model by feeding chickens diets containing different amounts of Cu. In the present study, histopathological observations have revealed morphological damage to the jejunum. The expression levels of genes and proteins of intestinal barrier markers were prominently downregulated. While the mRNA expression level of the gene associated with CYP450s was significantly increased. Additionally, apoptosis-related genes and proteins (Bak1, Bax, Caspase-9, Caspase-3, and CytC) were also significantly augmented by excessive Cu, while simultaneously decreasing the expression of Bcl-2. It can be concluded that long-term Cu exposure affects CYP450s activity, disrupts intestinal barrier function, and causes apoptosis in broilers that ultimately leads to jejunum damage.

Copper (Cu), an omnipresent environmental pollutant, can cause potential harm to the public and ecosystems. In order to study the cardiotoxicity caused by Cu, molecular biology techniques were used to analyze the effect of Cu on ER stress-mediated cardiac apoptosis. In vivo investigation, 240 1-day-old chickens were fed with Cu (11, 110, 220, and 330 mg/kg) diet for 7 weeks. The consequence showed that high-Cu can induce ER stress and apoptosis in heart tissue. The vitro experiments, the Cu treatment for 24 h could provoke ultrastructural damage and upregulate the apoptosis rate. Meanwhile, GRP78, GRP94, eIF2α, ATF6, XBP1, CHOP, Bax, Bak1, Bcl2, Caspase-12 and Caspase-3 genes levels, and GRP78, GRP94 and Caspase-3 proteins levels were increased, which indicated that ER stress and apoptosis in cardiomyocytes. But the mRNA level of Bcl2 were decreased after Cu exposure. Conversely, Cu-induced ER stress-mediated apoptosis can be alleviated by treatment with 4-PBA. These findings generally showed that Cu exposure can contribute to ER stress-mediated apoptosis in chicken myocardium, which clarifies the important mechanism link between ER stress and apoptosis, and provides a new perspective for Cu toxicology.

Copper (Cu) is one of the common heavy metal pollutants in the environment, and its toxic mechanisms have been extensively studied. However, the immunotoxicity induced by Cu remains rarely reported, and the effects of Cu on endoplasmic reticulum stress and mitochondria-mediated apoptosis have been little studied in the spleen. In this study, pigs were fed with different contents of Cu (10, 125, and 250 mg/kg Cu) for 80 days to establish a toxicity model. The results showed the Cu exposure triggered endoplasmic reticulum stress in the spleen, as evidenced by increased mRNA and protein levels of GRP94, GRP78, CHOP, XBP1, ATF6, and JNK; the positive rate of GRP78 increased by immunofluorescence analysis. Additionally, mitochondrial fission and fusion homeostasis were disrupted, the expression levels of mitochondrial dynamics–related genes Mfn1, Mfn2, and OPA1 decreased, DRP1 increased, and the positive rate of Mfn1 decreased by immunofluorescence analysis. Furthermore, Cu exposure could induce apoptosis, as demonstrated by the increased expression level of related proteins and genes Bak, Bax, Caspase-3, P53, and Cytc. In conclusion, these results suggest chronic Cu exposure can lead to endoplasmic reticulum stress and imbalance in mitochondrial dynamics and induced apoptosis of pig spleen, and these results provided new insights into the underlying mechanism of Cu exposure caused splenic toxicity, which has public health implications where humans and animals are exposed to copper contamination.