A New Insight into the Mechanism of Atrazine-Induced Neurotoxicity: Triggering Neural Stem Cell Senescence by Activating the Integrated Stress Response Pathway.

Atrazine (AT), a widely utilized chemical herbicide, causes widespread contamination of agricultural water bodies. Recently, exposure to AT has been linked to the development of age-related neurodegenerative diseases (NDs), suggesting its neurotoxicity potential. As an endocrine disruptor, AT targets the hypothalamus, a crucial part of the neuroendocrine system.

Deltamethrin exposure caused renal inflammation and renal fibrosis via upregulating endoplasmic reticulum stress-mediated TXNDC5 level in mice.

Deltamethrin (DLM) is a type II pyrethroid insecticide that is extensively applied to agriculture, veterinary medicine and livestock pest control. Excessive accumulation of DLM in the body can lead to nephrotoxicity, but the precise toxic mechanism remains obscure. Therefore, we established in vivo models of DLM-exposed mice for 30 days and in vitro models of DLM-exposed renal tubular epithelial cells of mice.

Comparative mitochondrial proteomic: PGAM5-mediated necroptosis through excessive mitophagy in sheep livers under molybdenum and cadmium co-exposure.

Accumulation of excessive molybdenum (Mo) and cadmium (Cd) in the environment poses detrimental effects on organisms. The precise mechanisms of hepatotoxicity that are involved with mitochondria, resulting from the co-exposure to Mo and Cd, remain poorly understood and elusive. To fill the gap, a total of 24 sheep were stratified into two groups: control group and Mo + Cd group (45 mg Mo·kg⁻¹·B.

Ginkgo biloba extract alleviates deltamethrin-induced testicular injury by upregulating SKP2 and inhibiting Beclin1-independent autophagy.

Background: Male infertility is a worldwide concern that is associated with a decline in sperm quality. Environmental pollutants such as deltamethrin (DM) have harmful effects on male reproductive organs. By maintaining intracellular redox homeostasis, ginkgo biloba extract (GBE) can alleviate male reproductive dysfunction.

Activating PPARβ/δ-Mediated Fatty Acid β-Oxidation Mitigates Mitochondrial Dysfunction Co-induced by Environmentally Relevant Levels of Molybdenum and Cadmium in Duck Kidneys.

Cadmium (Cd) and high molybdenum (Mo) pose deleterious effects on health. Prior studies have indicated that exposure to Mo and Cd leads to damage in duck kidneys, but limited studies have explored this damage from the perspective of fatty acid metabolism. In this study, 40 healthy 8-day-old ducks were randomly assigned to four groups and fed a basic diet containing Cd (4 mg/kg Cd) or Mo (100 mg/kg Mo) or both.

Copper as the driver of the lncRNA-TCONS-6251/miR-novel-100/TC2N axis: Unraveling ferroptosis in duck kidney.

Ferroptosis is an iron-dependent form of oxidative cell death. Competitive endogenous RNAs diminish the inhibitory impact of microRNAs on other transcripts by chelating effects, which affects ferroptosis and reactive oxygen species (ROS) levels. However, the role of ferroptosis in excessive copper (Cu)-induced renal injury via the ceRNA axis has not been fully illustrated yet.

Lycopene mitigates atrazine-induced hypothalamic neural stem cell senescence by modulating the integrated stress response pathway.

Background: Atrazine, a widely used herbicide, has become a major pollutant in agricultural water bodies. Pesticide contamination, including atrazine, is linked to a high incidence of age-related neurodegenerative diseases, suggesting its neurotoxic potential. Lycopene, a potent antioxidant, is renowned for its diverse pharmacological effects, especially its neuroprotective properties.

Cooperative application of transcriptomics and ceRNA hypothesis: lncRNA-00742/miR-116 targets CD74 to mediate vanadium-induced mitochondrial apoptosis in duck liver.

Vanadium (V) is a poisonous metallic environmental pollutant which poses hazard to the animal health of the liver. Competitive endogenous ribonucleic acids (ceRNAs) are essential elements of mitochondrial function and apoptosis, and their effects have been associated with the metal toxicity mechanism. However, the specific mechanism of ceRNAs in V-induced mitochondrial apoptosis in the liver has not been adequately investigated.

Identification and phylogenetic analysis of Jingmen tick virus in Jiangxi Province, China.

Jingmen tick virus (JMTV) is a newly identified segmented flavivirus that has been recognized in multiple hosts, such as humans, buffalos, bats, rodents, mosquitos and ticks. Various clinical cases and studies manifested that JMTV is a true arbovirus with wide host spectrum and showed potential threats toward public health. JMTV has been reported in multiple countries in Asia, Europe, Africa, and America.

Environmentally relevant levels of Cd and Mo coexposure induces ferroptosis and excess ferritinophagy through AMPK/mTOR axis in duck myocardium.

Cadmium (Cd) and excess molybdenum (Mo) are multiorgan toxic, but the detrimental impacts of Cd and/or Mo on poultry have not been fully clarified. Thence, a 16-week sub-chronic toxic experiment was executed with ducks to assess the toxicity of Cd and/or Mo. Our data substantiated that Cd and Mo coexposure evidently reduced GSH-Px, GSH, T-SOD, and CAT activities and elevated HO and MDA concentrations in myocardium.

Molybdenum and cadmium co-induce apoptosis and ferroptosis through inhibiting Nrf2 signaling pathway in duck (Anas platyrhyncha) testes.

Cadmium (Cd) and high molybdenum (Mo) are injurious to the body. Previous research has substantiated that Cd and Mo exposure caused testicular injury of ducks, but concrete mechanism is not fully clarified. To further survey the toxicity of co-exposure to Cd and Mo in testis, 40 healthy 8-day-old Shaoxing ducks (Anas platyrhyncha) were stochasticly distributed to 4 groups and raised with basic diet embracing Cd (4 mg/kg Cd) or Mo (100 mg/kg Mo) or both.

Molybdenum and cadmium co-induce necroptosis through Th1/Th2 imbalance-mediated endoplasmic reticulum stress in duck ovaries.

Cadmium (Cd) and excess molybdenum (Mo) pose serious threats to animal health. Our previous study has determined that Cd and/or Mo exposure can cause ovarian damage of ducks, while the specific mechanism is still obscure. To further investigate the toxic mechanism of Cd and Mo co-exposure in the ovary, forty 8-day-old female ducks were randomly allocated into four groups for 16 weeks, and the doses of Cd and Mo in basic diet per kg were as follows: control group, Mo group (100 mg Mo), Cd group (4 mg Cd), and Mo + Cd group (100 mg Mo + 4 mg Cd).

Role of the GLP2-Wnt1 axis in silicon-rich alkaline mineral water maintaining intestinal epithelium regeneration in piglets under early-life stress.

Stress-induced intestinal epithelial injury (IEI) and a delay in repair in infancy are predisposing factors for refractory gut diseases in adulthood, such as irritable bowel syndrome (IBS). Hence, it is necessary to develop appropriate mitigation methods for mammals when experiencing early-life stress (ELS). Weaning, as we all know, is a vital procedure that all mammalian newborns, including humans, must go through.

Co-exposure to Environmentally Relevant Levels of Molybdenum and Cadmium Induces Oxidative Stress and Ferroptosis in the Ovary of Ducks.

Excessive doses of molybdenum (Mo) and cadmium (Cd) have toxic effects on animals. Nevertheless, the reproductive toxicity elicited by Mo and Cd co-exposure remains obscure. To evaluate the co-induce toxic impacts of Mo and Cd on ovaries, 8-day-old 40 healthy ducks were stochastically distributed to four groups and were raised a basal diet supplemented with Cd (4 mg/kg Cd) and/or Mo (100 mg/kg Mo).

Mitochondria-associated endoplasmic reticulum membrane as a mediator of vanadium-induced endoplasmic reticulum quality control in duck brains.

Vanadium (V) plays a crucial role in normal cells, but excess V causes multi-organ toxicity, including neurotoxicity. Mitochondria-associated endoplasmic reticulum membrane (MAM) is a dynamic structure between endoplasmic reticulum (ER) and mitochondria that mediates ER quality control (ERQC). To explore the effects of excess V on MAM and ERQC in the brain, 72 ducks were randomly divided into two groups: the control group (basal diet) and the V group (30 mg V/kg basal diet).

MAPK/NF-κB signaling mediates atrazine-induced cardiorenal syndrome and antagonism of lycopene.

Atrazine (ATZ) is the most prevalent herbicide that has been widely used in agriculture to control broadleaf weeds and improve crop yield and quality. The heavy use of ATZ has caused serious environmental pollution and toxicity to human health. Lycopene (LYC), is a carotenoid that exhibits numerous health benefits, such as prevention of cardiovascular diseases and nephropathy.

Berberine Protects against High-Energy and Low-Protein Diet-Induced Hepatic Steatosis: Modulation of Gut Microbiota and Bile Acid Metabolism in Laying Hens.

Berberine (BBR) is a natural alkaloid with multiple biotical effects that has potential as a treatment for fatty liver hemorrhagic syndrome (FLHS). However, the mechanism underlying the protective effect of BBR against FLHS remains unclear. The present study aimed to investigate the effect of BBR on FLHS induced by a high-energy, low-protein (HELP) diet and explore the involvement of the gut microbiota and bile acid metabolism in the protective effects.

Hexavalent-Chromium-Induced Disruption of Mitochondrial Dynamics and Apoptosis in the Liver via the AMPK-PGC-1α Pathway in Ducks.

Hexavalent chromium (Cr(VI)) is a hazardous substance that poses significant risks to environmental ecosystems and animal organisms. However, the specific consequences of Cr(VI) exposure in terms of liver damage remain incompletely understood. This study aims to elucidate the mechanism by which Cr(VI) disrupts mitochondrial dynamics, leading to hepatic injury in ducks.

Prenatal cadmium exposure impairs neural tube closure via inducing excessive apoptosis in neuroepithelium.

Birth defects have become a public health concern. The hazardous environmental factors exposure to embryos could increase the risk of birth defects. Cadmium, a toxic environmental factor, can cross the placental barrier during pregnancy.

Molybdenum exposure induces inflammatory response via the regulatory effects of lncRNA-00072124/miR-308/OSMR crosstalk on JAK/STAT axis in duck kidneys.

Molybdenum (Mo) is an essential nutrient in living organisms. Although numerous researchers have noticed the health damage caused by excessive Mo, the underlying mechanism of excessive Mo-induced nephrotoxicity remains poorly understood. A gene crosstalk called competitive endogenous RNAs (ceRNAs) can interpret many regulatory mechanisms molecularly.

Inhibition of calcium imbalance protects hepatocytes from vanadium exposure-induced inflammation by mediating mitochondrial-associated endoplasmic reticulum membranes in ducks.

Vanadium (V) is an essential mineral element in animals, but excessive V can lead to many diseases, affecting the health of humans and animals. However, the molecular crosstalk between mitochondria-associated endoplasmic reticulum membranes (MAMs) and inflammation under V exposure is still at the exploratory stage. This study was conducted to determine the molecular crosstalk between MAMs and inflammation under V exposure in ducks.

Molybdenum and cadmium cause blood-testis barrier dysfunction through ROS-mediated NLRP3 inflammasome activation in sheep.

In this study, 24 healthy male sheep were divided into four groups: the control group, Mo group (45 mg Mo·kg-1·BW), Cd group (1 mg Cd·kg-1·BW), and Mo + Cd group (45 mg Mo·kg-1·BW + 1 mg Cd·kg-1·BW). The experiment was last for 50 d. The results showed that Mo and Cd co-exposure induced histopathological changes and ultrastructural damage, decreased the mRNA and protein expression levels of BTB (blood-testis barrier)-related factors (CX-43, ZO-1, OCLN) (P < 0.

Unexpected worker mating and colony-founding in a superorganism.

The emergence of caste-differentiated colonies, which have been defined as 'superorganisms', in ants, bees, and wasps represents a major transition in evolution. Lifetime mating commitment by queens, pre-imaginal caste determination and lifetime unmatedness of workers are key features of these animal societies. Workers in superorganismal species like honey bees and many ants have consequently lost, or retain only vestigial spermathecal structures.

Role of PLC/IP /IP R axis in excess molybdenum exposure induced apoptosis in duck renal tubular epithelial cells.

Excess molybdenum (Mo) is harmful to animals, but its nephrotoxicity has not been comprehensively explained. To appraise the influences of excess Mo on Ca homeostasis and apoptosis via PLC/IP /IP R axis, primary duck renal tubular epithelial cells were exposed to 480 μM and 960 μM Mo, and joint of 960 μM Mo and 10 μM 2-APB or 0.125 μM U-73122 for 12 h (U-73122 pretreated for 1 h), respectively.