Analysis of 28 trace elements in the blood and serum antioxidant status in chickens under arsenic and/or copper exposure.

This study aimed to evaluate the 28 trace elements in the blood and serum antioxidant status in chickens under arsenic (As) and/or copper (Cu) exposure. A total of 200 1-day-old male Hy-Line chickens were fed either a commercial diet (C-group) or arsenic trioxide (30 mg/kg) and/or cupric sulfate (300 mg/kg) for 90 days. The 28 trace element levels in the blood were analyzed by inductively coupled plasma mass spectrometry (ICP-MS). The concentrations of As in the blood of chickens were elevated approximately 17.15-fold, 2.30-fold, and 13.37-fold in the As-group, Cu-group, and As + Cu-group, respectively, at 90 days. The concentrations of Cu did not change in the As-group and increased approximately 29.53 and 23.37% in the Cu-group and As + Cu-group, respectively, at 90 days. Moreover, As exposure caused ion profile disorders in the blood, including increased concentrations of Na, Mg, Si, K, Cr, Fe, and Se and reduced B, Ca, Ti, V, Mn, Co, Ni, Zn, Sr, and Mo. Cu exposure increased the contents of Mg, Si, Ca, Ti, V, Cr, Mn, Fe, Co, Zn, and Se and decreased the content of B, Ca, Al, Ni, and Mo. As + Cu exposure increased the contents of Mg, Si, Cr, Fe, Zn, and Se and decreased the content of B, Ca, Ti, Co, Ni, Sr, and Mo. Moreover, As and/or Cu exposure induced oxidative stress in the blood of chickens. In conclusion, the results indicated that the mixture of As and Cu caused a synergistic effect via disturbing homeostasis of trace elements and oxidative stress in the blood of chickens.

Assessment of arsenic trioxide toxicity on cock muscular tissue: alterations of oxidative damage parameters, inflammatory cytokines and heat shock proteins.

To evaluate the toxicity of arsenic trioxide (As2O3) in the muscular tissues (wing, thigh and pectoral) of birds, 72 one-day-old Hy-line cocks were selected and randomly divided into four groups. They were fed either a commercial diet or an arsenic-supplemented diet containing 7.5, 15 or 30 mg/kg As2O3. The experiment lasted for 90 days and the samples of muscular tissues were collected at 30, 60 and 90 days. The results showed that As2O3 exposure significantly lowered the activities of antioxidant enzymes (catalase (CAT), glutathione peroxidase (GSH-Px)) and inhibition ability of hydroxyl radicals (OH) and increased the malondialdehyde (MDA) contents. Furthermore, the mRNA levels of inflammatory cytokines (tumor necrosis factor-α (TNF-α), nuclear factor-kappa B (NF-κB), cyclooxygenase-2 (COX-2), inducible NO synthase (iNOS), prostaglandin E synthase (PTGEs)) and heat shock proteins (HSPs) in muscular tissue were significantly upregulated in the As2O3 exposure groups. The results indicated that As2O3 exposure resulted in oxidative damage, induced the inflammatory response, and influenced the mRNA levels of HSPs in muscular tissue of cocks. Additionally, the results suggested that HSPs possibly resisted due to the As2O3 exposure-induced oxidative stress and inflammatory response, which provided a favorable environment and played protective roles in the muscular tissues of cocks. The information presented in this study is helpful to understand the mechanism of As2O3 toxicity in bird muscular tissues.

Assessment of 28 trace elements and 17 amino acid levels in muscular tissues of broiler chicken (Gallus gallus) suffering from arsenic trioxide.

The contents of 28 trace elements, 17 amino acid were evaluated in muscular tissues (wings, crureus and pectoralis) of chickens in response to arsenic trioxide (As2O3). A total of 200 one-day-old male Hy-line chickens were fed either a commercial diet (C-group) or an As2O3 supplement diet containing 7.5mg/kg (L-group), 15mg/kg (M-group) or 30mg/kg (H-group) As2O3 for 90 days. The elements content was analyzed by inductively coupled plasma mass spectrometry (ICP-MS). Under As2O3 exposure, the concentration of As were elevated 8.87-15.76 fold, 7.93-15.63 fold and 5.94-12.45 fold in wings, crureus and pectoralis compared to the corresponding C-group, respectively. 19 element levels (lithium (Li), magnesium (Mg), aluminum (Al), silicon (Si), kalium (K), vanadium (V), chromium (Cr), manganese (Mn), nickel (Ni), copper (Cu), selenium (Se), strontium (Sr), molybdenum (Mo), cadmium (Cd), tin (Sn), antimony (Sb), barium (Ba), mercury (Hg) and lead (Pb), 9 element levels (K, Co, Ni, Cu, As, Se, Sr, Sn, Ba and Hg) and 4 element levels (Mn, cobalt (Co), As, Sr and Ba) were significantly increased (P < 0.05) in wing, crureus and pectoralis, respectively. 2 element levels (sodium (Na) and zinc (Zn)), 5 element levels (Li, Na, Si, titanium (Ti and Cr), 13 element levels (Li, Na, Mg, K, V, Cr, iron (Fe), Cu, Zn, Mo, Sn, Hg and Pb) were significantly decreased (P < 0.05) in wing muscle, crureus and pectoralis, respectively. Additionally, in crureus and pectoralis, the content of total amino acids (TAA) was no significant alterations in L and M-group and then increased approximately 10.2% and 7.6% in H-group, respectively (P < 0.05). In wings, the level of total amino acids increased approximately 10% in L-group, whereas it showed unchanged in M and H-group compared to the corresponding C-group. We also observed that significantly increased levels of proline, cysteine, aspartic acid, methionine along with decrease in the tyrosine levels in muscular tissues compared to the corresponding C-group. In conclusion, the residual of As in the muscular tissues of chickens were dose-dependent and disrupts trace element homeostasis, amino acids level in muscular tissues of chickens under As2O3 exposure. Additionally, the response (trace elements and amino acids) were different in wing, thigh and pectoral of chick under As2O3 exposure. This study provided references for further study of heavy metal poisoning and may be helpful to understanding the toxicological mechanism of As2O3 exposure in muscular tissues of chickens.

Assessment of arsenic trioxide in the heart of Gallus gallus: alterations of oxidative damage parameters, inflammatory cytokines, and cardiac enzymes.

The aim of this study was to assess the effects of arsenic trioxide (As2O3) in the chicken heart, and 72 1-day-old male Hy-line chickens were fed either a commercial diet (C group) or an arsenic supplement diet containing 7.5 mg/kg (L group), 15 mg/kg (M group), or 30 mg/kg (H group) As2O3 for 90 days. The results showed that exposure to As2O3 merely lowered (P < 0.05) the activities of catalase (CAT) and glutathione peroxidase (GSH-Px) in M and H groups at 90 days, significantly downregulated the inhibition ability of hydroxyl radicals (OH·), and upregulated (P < 0.05) the contents of malondialdehyde (MDA) in As2O3 exposure groups at 30, 60, and 90 days. Meanwhile, the messenger RNA levels of inflammatory cytokines (tumor necrosis factor-α (TNF-α), nuclear factor-kappa B (NF-κB), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and prostaglandin E synthase (PTGEs)) significantly increased (P < 0.05) in As2O3 exposure groups at 30, 60, and 90 days, and histological and ultrastructural damage was observed in As2O3 exposure groups. Additionally, As2O3-induced cardiac enzyme (aspartate transaminase (AST), creatine kinase (CK), creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and α-hydroxybutyrate dehydrogenase (α-HBDH)) levels increased (P < 0.05) at 90 days. These findings suggested that As2O3 exposure led to oxidative stress, inflammatory response, and histological and ultrastructural damage and altered the levels of cardiac enzymes in chicken heart tissues. This result may be helpful for further studies on the toxicological mechanisms of As2O3 in the chicken heart.

Influence of inflammatory pathway markers on oxidative stress induced by cold stress in intestine of quails.

The cold temperature reduces the immunity and re-production activities of the poultry. This study aimed to investigate the effects of acute and chronic cold exposure on the regulation of nuclear factor-kappa B (NF-κB) and tumor necrosis factor-α (TNF-α) expression in the duodenum, jejunum, and ileum of quails. In this study, 96 15-d-old male quails were randomly allocated into 12 groups (eight each group) for exposure to acute (up to 12h) and chronic (up to 20 days) cold stress (12 ± 1°C). Antioxidative function was examined by superoxide dismutase (SOD) and oxidative damage was examined by malondialdehyde (MDA) detection. qRT-PCR was performed to analyze expression of NF-κB and TNF-α, and DNA sequencing was performed to analyze PCR products. The data showed that under cold stress, the SOD level decreased, and the MDA level had the tendency to increase in duodenum, jejunum and ileum of quails, while the mRNA expression of NF-κB increased and TNF-α decreased in duodenum, jejunum and ileum of quails. The data from the current study indicated that both acute and chronic cold stresses were able to induce inflammatory responses in the duodenum, jejunum and ileum, which might be due to the cold-damaged intestinal oxidative stress.