Transport Stress Induced Cardiac NO-NOS Disorder Is Mitigated by Activating Nrf2/HO-1/NQO1 Antioxidant Defense Response in Newly Hatched Chicks.

With the development of the intensive poultry industry, the health problems of chickens caused by transportation have attracted more and more attention. Transport stress reduces performance, immune function, and meat quality in chicks, which has become one of the most important factors that endanger the development of the poultry industry. Currently, studies on the effects of transport stress have mainly focused on the performance of livestock and poultry to be slaughtered. However, the effects of transport stress on heart damage and oxidative stress in newborn chicks have not been reported. In this study, we selected newborn chicks as the object. This study was intended to explore the effects of transport stress on the heart damage of newly hatched chicks. The findings suggested that transport stress could cause oxidative stress in the hearts of newly hatched chicks by increasing the levels of malondialdehyde (MDA), hydrogen peroxide (H2O2) and decreasing the contents of Total antioxidant capacity (T-AOC), and the activities of antioxidant enzymes (SOD), together with increasing the activities of antioxidant enzymes (Catalase (CAT) and Glutathione S-transferase (GST)). Transport stress disrupted the balance between oxidation and antioxidant systems. The Nrf2 signaling pathway was activated by transport stress and triggered the transcription of antioxidant signaling. In short, transport stress-induced nitric oxide (NO)-nitric oxide synthases (NOS) system metabolic disorders and cardiac oxidative stress are mitigated by activating the nuclear factor-erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1)/NAD(P)H quinone oxidoreductase-1 (NQO1) antioxidant defense response in newly hatched chicks.

Lycopene prevents DEHP-induced hepatic oxidative stress damage by crosstalk between AHR-Nrf2 pathway.

Di (2-ethylhexyl) phthalate (DEHP) is a widespread plasticizer that persists in the environment and can significantly contribute to serious health hazards of liver especially oxidative stress injury. Lycopene (LYC) as a carotenoid has recently gained widespread attention because of antioxidant activity. However, the potential mechanism of DEHP-induced hepatotoxicity and antagonism effect of LYC on it are still unclear. To explore the underlying mechanisms of this hypothesis, the mice were given by gavage with LYC (5 mg/kg) and DEHP (500 or 1000 mg/kg). The data suggested that DEHP caused liver enlargement, reduction of antioxidant activity markers, increase of oxidative stress indicators and disorder of cytochrome P450 enzymes system (CYP450s) homeostasis. DEHP-induced reactive oxygen species (ROS) activated the NF-E2-relatedfactor2 (Nrf2) and nuclear xenobiotic receptors (NXRs) system including Aryl hydrocarbon receptor (AHR), Pregnane X receptor (PXR) and Constitutive androstane receptor (CAR). Interestingly, these disorders and injuries were prevented after LYC treatment. Taken together, DEHP administration resulted in hepatotoxicity including oxidative stress injury and disordered CYP450 system, but these alterations might be ameliorated by LYC via crosstalk between AHR-Nrf2 pathway.

Th1/Th2 imbalance and heat shock protein mediated inflammatory damage triggered by manganese via activating NF-κB pathway in chicken nervous system in vivo and in vitro.

Manganese (Mn) is a ubiquitous heavy metal pollutant in environment, and excess Mn can damage nervous system of humans and animals. However, molecular mechanism of Mn-induced poultry neurotoxicity on inflammatory injury is still not fully clear. Thus, the purpose of the conducted research was to explore molecular mechanism of inflammatory injury caused by Mn in chicken nervous system. Two Mn poisoning models were established in vivo and in vitro. One hundred and eighty chickens were randomly separated into four groups. One control group was raised drinking water and standard diet. Three Mn groups were raised drinking water, and the standard diet supplemented with three different concentrations of MnCl2 ∙ 4H2O. There were 45 birds and 3 replicates in each group. Neurocytes from chicken embryos were cultured in mediums without and with six different concentrations of MnCl2 ∙ 4H2O in vitro. Our experiments showed that excess Mn caused cerebral histomorphological structure alternations and damage, and increased the expressions (P < 0.05) of inflammation-related factor NF-κB, TNF-α, iNOS, COX-2, and PTGEs in vivo and in vitro, meaning that excess Mn caused inflammatory damage and inflammatory response in chicken nervous system. Moreover, there were an upregulated IFN-γ mRNA expression and a downregulated IL-4 mRNA expression (P < 0.05) in bird cerebra and embryonic neurocytes after exposure to Mn, indicating that Mn exposure caused Th1/Th2 imbalance and immunosuppression. Additionally, in our research, the elevation (P < 0.05) of five HSPs (HSP27, HSP40, HSP60, HSP70, and HSP90) was found, suggesting that HSPs participated molecular mechanism of Mn stress. In addition, the inflammatory toxicity of Mn to chicken nervous system was time- and dose-dependent. Taken all together, our findings indicated that Th1/Th2 imbalance and HSPs mediated Mn-caused inflammatory injury via NF-κB pathway in chicken nervous system in vivo and in vitro.

Endogenous Hydrogen Sulfide Promotes Apoptosis via Mitochondrial Pathways in the Livers of Broilers with Selenium Deficiency Exudative Diathesis Disease.

Hydrogen sulfide (H2S), an endogenous gasotransmitter, plays an important role in apoptosis. Exudative diathesis (ED) disease is associated with dietary selenium (Se) deficiency in broilers. The liver is one of the target organs of Se deficiency; however, little is known about the effect of H2S on apoptosis via mitochondrial pathways in the livers of broilers with ED disease. In the present study, we aimed to investigate the correlation between endogenous H2S and mitochondrial-mediated apoptosis in the livers of broilers with ED disease, as induced by Se deficiency. One hundred twenty healthy, 1-day-old broilers were randomly assigned to one of two groups (60 each) based on diet: Basal diet (control group, 0.2 mg/kg Se) or a low-Se diet (-Se group, 0.033 mg/kg Se). At day 20, 15 broilers of a similar weight were sacrificed from the control group, while the same number of broilers were euthanatized from the -Se group when displaying typical symptoms of ED between days 18 and 25. The livers were collected, and apoptosis was measured using a TUNEL assay. Additionally, H2S concentration, the expression of H2S synthases of cystathionine γ-lyase (CSE), cystathionine ß-synthase (CBS), and 3-mercaptopyruvate sulfurtransferase (3-MST), as well as mitochondrial apoptosis-related genes of Bcl-2, Bax, Bak, Cyt-C, Caspase-9, Caspase-3, and p53, were examined in livers. The results indicated that Se deficiency could induce apoptosis in the livers of broilers. Swelling, fractures, and vacuolization were visible in the mitochondrial cristae in the livers of the -Se group. The expression of H2S synthase-related genes and H2S concentration was significantly enhanced (P < 0.05) in the livers of the -Se group compared to controls. Moreover, a low-Se diet downregulated (P < 0.05) the level of Bcl-2 and upregulated (P < 0.05) the levels of Bax, Bak, Cyt-C, Caspase-9, Caspase-3, and p53. These results suggest that an H2S increase in the livers of ED broilers, which was induced by Se deficiency, is related to apoptosis mediated by mitochondrial pathways.

Selenium Supplementation Changes the Ion Profile in the Pancreas of Chickens Treated with Cadmium.

Increasing evidence indicates that selenium (Se) could antagonize metal toxicity, including cadmium (Cd) toxicity. However, the effects of Se on Cd-induced changes in the ion profile in the pancreas of chickens have not been reported. In the present study, 128 Hy-Line brown laying chickens were divided into the control group, Se-treated group, Se/Cd-treated group, and Cd-treated group, and we detected the concentrations of 28 ions in the four groups by inductively coupled plasma mass spectrometry. In the Cd-treated group, the accumulation of Cd in the pancreas was 836.8 times higher that than in the control group (27,353.71 ppb/32.69 ppb). Meanwhile, the Ca, Ti, Fe, Mo, Li, Al, and Pb levels increased and the Cr, Mn, Ni, Cu, Zn, Se, Sr, and Sb levels decreased due to sub-chronic Cd poisoning. The Fe, Mo, Ba, and Pb levels decreased in the Se/Cd-treated group. Our findings suggest that Cd can accumulate in the chicken pancreas and affect the ion profiles, whereas Se can ameliorate the accumulation of Cd and change the ion profiles in the chicken pancreas.

The Antagonistic Effect of Selenium on Cadmium-Induced Damage and mRNA Levels of Selenoprotein Genes and Inflammatory Factors in Chicken Kidney Tissue.

Selenium (Se) is a necessary trace mineral in the diet of humans and animals. Cadmium (Cd) is a toxic heavy metal that can damage animal organs, especially the kidneys. Antagonistic interactions between Se and Cd have been reported in previous studies. However, little is known about the effects of Se against Cd toxicity and on the mRNA levels of 25 selenoprotein genes and inflammatory factors in chicken kidneys. In the current study, we fed chickens with a Se-treated, Cd-treated, or Se/Cd treated diet for 90 days. We then analyzed the mRNA expression of inflammatory factors (including prostaglandin E synthase (PTGES), nuclear factor-kappa B (NF-κB), tumor necrosis factor-α (TNF-α), and cyclooxygenase-2 (COX-2)) and 25 selenoprotein genes (Gpx1, Gpx2, Gpx3, Gpx4, Txnrd1, Txnrd2, Txnrd3, Dio1, Dio2, Dio3, SPS2, Sepp1, SelPb, Sep15, Selh, Seli, Selm, Selo, Sels, Sepx1, Selu, Selk, Selw, Seln, Selt). The results demonstrated that Cd exposure increased the Cd content in the chicken kidneys, renal tubular epithelial cells underwent denaturation and necrosis, and the tubules became narrow or disappeared. However, Se supplementation reduced the Cd content in chicken kidneys and induced normal development of renal tubular epithelial cells. In addition, we also observed that Se alleviated the Cd-induced increase in the mRNA levels of inflammatory factors and ameliorated the Cd-induced downtrend in the mRNA levels of 25 selenoprotein genes in chicken kidneys.

Selenium protects against cadmium-induced kidney apoptosis in chickens by activating the PI3K/AKT/Bcl-2 signaling pathway.

Cadmium (Cd) is a toxic heavy metal that can induce apoptosis. Selenium (Se) is a necessary trace element and can antagonize the toxicity of many heavy metals, including Cd. PI3K/AKT/Bcl-2 is a key survival signaling pathway that regulates cellular defense system against oxidative injury as well as cell proliferation, survival, and apoptosis. The antagonistic effects of Se on Cd-induced toxicity have been reported. However, little is known about the effect of Se on Cd-induced apoptosis in chicken kidneys via the PI3K/AKT/Bcl-2 signaling pathway. In the present study, we fed chickens with Se, Cd, or both Se and Cd supplements, and after 90 days of treatment, we detected the related index. The results showed that the activity of inducible nitric oxide synthase (iNOS) and concentration of nitric oxide (NO) were increased; activities of the mitochondrial respiratory chain complexes (complexes I, II, and V) and ATPases (the Na+-K+-ATPase, the Mg2+-ATPase, and the Ca2+-ATPase) were decreased; expression of PI3K, AKT, and Bcl-2 were decreased; and expression of Bax, Bak, P53, Caspase-3, Caspase-9, and cytochrome c (Cyt c) were increased. Additionally, the results of the TUNEL assay showed that the number of apoptotic cells was increased in the Cd group. By contrast, there was a significant improvement of the correlation indicators and occurrence of apoptosis in the Se + Cd group compared to the Cd group. In conclusion, our results confirmed that Se had a positive effect on ameliorating Cd-induced apoptosis in chicken kidney tissue by activating the PI3K/AKT/Bcl-2 signaling pathway.