Broilers' head behavior as an early warning index of production and lung health under ammonia exposure.

This study investigated the effects of ammonia exposure (0, 15, 25, and 35 ppm) on head behavior, production performance and lung tissue morphology of broilers, and the relationship between head behavior, production performance, and lung tissue injury. In this experiment, a total of 264 AA commercial male broilers (21 d old) were assigned to 4 treatment groups with 6 replicates of 11 chickens for a 21-day trial period, the frequency of head-scratching and head-shaking behavior at the initial stage (2, 24, and 72 h) of ammonia exposure were recorded, and the production performance indices and the lung pathological changes after 21 d of ammonia exposure were observed. The correlation analysis was established between head behavior and production performance indices. Results showed that head-scratching behavior increased under 15 ppm ammonia for 72 h, head-shaking behavior increased when exposure to 15 ppm ammonia for 2, 24, and 72 h, and lung tissue was injured when exposure to 15 ppm ammonia for 21 d. However, exposure to 15 ppm ammonia did not influence growth performance. Compared with the control group, exposure to 25 ppm decreased the ADG and exposure to 35 ppm decreased the ADG, ADFI, and F/G. Furthermore, the increase in head-shaking frequency after 2 h and 24 h ammonia exposure was significantly associated with production performance and lung tissue injury after 21 d ammonia exposure. In conclusion, the head-shaking behavior at the initial stage of ammonia exposure can reflect the degree of harm of the later production performance and lung tissue health.

Ammonia induce lung tissue injury in broilers by activating NLRP3 inflammasome via Escherichia/Shigella.

Respiratory tract diseases are closely related to atmosphere pollution. Ammonia is one of the harmful pollutants in the atmosphere environment, which has a great threat to human and animal respiratory tract health, but the mechanism of causing diseases is not clear. In this study, broiler lung tissue was used as a model to study the effect of high ammonia on respiratory tract diseases through the relationship between respiratory microflora, NLRP3 inflammasome, and inflammatory factors. For this, we validated the occurrence of lung tissue inflammation under ammonia exposure and detected the lung tissue microbial constituent by 16S rDNA sequencing. Moreover, the relative expression levels of NLRP3 and caspase-1 mRNA and the content of IL-1ß and IL-6 were measured. After 7-D ammonia exposure, the proportion of the phylum Proteobacteria and the genus Escherichia/Shigella in lung tissue was significantly increased, the expression levels of NLRP3 and caspase-1 mRNA were significantly increased, and the content of IL-1ß in lung tissue and serum was higher than that in the control group. In conclusion, high ammonia induced lung tissue inflammation via increasing the proportion of Escherichia/Shigella, activating NLRP3 inflammasome, and promoting IL-1ß release. These findings provided a reference for the prevention and control of respiratory tract diseases in humans and animals caused by ammonia pollution.

Effects of ammonia exposure on growth performance and cytokines in the serum, trachea, and ileum of broilers.

This study investigated the effects of ammonia (NH3) exposure (0, 15, 25, and 35 ppm) on growth performance and cytokines in the serum, trachea, and ileum of broilers. A total of 288 22-day-old male broiler chickens were assigned to 4 treatment groups with 6 replicates of 12 chickens for a 21-D trial period. Growth performance and cytokines (IL-1ß, IL-6, and IL-10) concentrations in the serum, trachea, and ileum were measured in response to 3, 7, 14, or 21 D of exposure to NH3. Correlations between cytokines in the serum, trachea, and ileum and growth performance, and between tracheal and ileal cytokines, were also analyzed. Results showed that exposure to 15 ppm NH3 did not influence the growth performance, but exposure to both 25 ppm and 35 ppm NH3 decreased the growth performance compared to that of the control group. Exposure to 15 ppm NH3 for 3 D increased IL-6 concentrations and induced an inflammatory response in the trachea and ileum, whereas exposure to 15 ppm NH3 for 7 D increased IL-10 concentrations and induced an anti-inflammatory response in the ileum. Exposure to 25 ppm NH3 induced an inflammatory response in the serum, trachea, and ileum after 3 D and induced an anti-inflammatory response in the ileum after 7 D. Exposure to 35 ppm NH3 for 3 D induced both inflammatory and anti-inflammatory responses in the trachea and ileum. Furthermore, increases in cytokines in the serum, trachea, or ileum were accompanied by a decrease in BW, ADFI, ADG, and an increase of feed/gain (F/G) from 7 D to 21 D. In addition, tracheal cytokine, especially IL-1ß, was positively correlated with ileal cytokine IL-1ß. These results indicated that the low growth performance associated with NH3 exposure may be due in part to an increase in cytokines, and the inflammatory response in the trachea and ileum may be related to cross-talk by cytokines such as IL-6, IL-10, and, in particular, IL-1ß.

Effects of stocking density on growth performance, growth regulatory factors, and endocrine hormones in broilers under appropriate environments.

Stocking density is an important environment factor that affects the development of poultry farming, which has caused widespread concern. This study was carried out to determine the effects of stocking density on growth performance, growth regulatory factors, and endocrine hormones in broilers under appropriate environments. A total of 144 Arbor Acres male broilers (BW 1000 ± 70 g) were randomly divided into low stocking density (LSD; 6.25 birds/m2), medium stocking density (MSD; 12.50 birds/m2), and high stocking density (HSD; 18.75 birds/m2) groups, with 6 replicates in each group, and raised in 3 environmental chambers (same size) from 29-day-old to 42-day-old, respectively. The trial period lasted for 14 D with 21 ± 1°C and 60 ± 7% relative humidity, wind speed < 0.5 m/s, ammonia level<5 ppm. The results indicated that average daily food intake and average daily gain in HSD group showed significantly lower than other 2 groups (P < 0.05). Besides, the HSD group significantly reduced breast muscle yield, tibial length, tibial width, and tibial weight of broilers (P < 0.05). The HSD group increased the mRNA expression level of myostatin, and reduced the mRNA expression levels of insulin-like growth factor 1 (IGF-1) and myogenic determination factor 1 (P < 0.05). The HSD group significantly reduced the expression of parathyroid hormone-related protein in tibial growth plate (P < 0.05). The HSD group increased the serum corticosterone levels of broilers (P < 0.05), and decreased the serum IGF-1 and thyroxine (T4) levels of broiler chickens (P < 0.05) than other stocking density groups. Moreover, the serum alkaline phosphatase levels were decreased (P < 0.05) with increasing stocking density, whereas there were no significant effects on the serum 3,5,3'-triiodothyronine (T3) concentrations in 3 groups (P > 0.05). In conclusion, under appropriate environments HSD reduced the growth performance of broilers and this negative effect was likely associated with decreased growth of muscle and bone.

Effects of chromium picolinate on oxidative damage in primary piglet hepatocytes.

Chromium picolinate is a popular nutritional supplement whose safety has been questioned because of the potential risk of oxidative DNA damage. To investigate this possibility, a dose-dependent study was performed in piglet hepatocyte cultures in which low (8 microM), medium (200 microM), and high (400 microM) doses of chromium picolinate were tested and compared to untreated controls. After 48 h incubation, there were no significant differences in the levels of intracellular reactive oxygen species, medium lactate dehydrogenase activity, and comet indicators between the three experimental groups and controls (p > 0.05). In the 8 microM-treated group, the intracellular malondialdehyde content was significantly decreased relative to controls (p < 0.05). All of the studied parameters showed a dose-dependent increase that was statistically significant between the low and high doses (p < 0.05). These results suggest that: (1) chromium picolinate may affect the oxidative status of piglet hepatocytes; (2) the appropriate dose (approximately physiological concentration) of chromium picolinate can inhibit lipid peroxidation, and (3) high doses of chromium picolinate have no significant effects on oxidative damage in piglet hepatocytes, but the existing evidence also imply that exposure to a higher dose appears to be unwarranted.

Study of oxidative damage in growing-finishing pigs with continuous excess dietary chromium picolinate intake.

Chromium picolinate (CrPic) is a popular nutritional supplement; however, its safety has been questioned as it may be a source of oxidative stress that induces genotoxicity. The current work investigated the effect of excessive CrPic intake on oxidative damage in growing-finishing pigs. Thirty castrated male pigs, weighing approximately 30 kg each, were randomly divided into five groups and fed a diet with 0, 200, 800, 1,600, 3,200 microg of Cr/kg feed as CrPic for 80 days (approximately the entire growing-finishing period). High CrPic dose significantly decreased superoxide dismutase activity in serum at 80 days as well as the catalase activity in kidney (p < 0.05); however, compared to controls, malondialdehyde in tissue and serum, urinary 8-hydroxydeoxyguanosine level, and DNA strand breaks in liver and kidney had no notable differences (p > 0.05). These results suggested that long-term exposure to different doses of CrPic in feed did not increase the formation of biomarkers of oxidative damage in growing-finishing pigs. However, taking into account the changes of antioxidant enzymes activity, excessive dietary CrPic intake was not recommended in this study.