RESUMO
Aerial ammonia exposure leads to tissue damage and metabolic dysfunction. However, it is unclear how different organs are coordinated to defend against aerial ammonia exposure. Twenty-four pigs were randomly divided into 4 groups, exposed to 0, 10, 25 or 35 mg/m3 ammonia respectively for 25 d. After above 25 mg/m3 ammonia exposure, decreased aspartate (P = 0.016), glutamate (P = 0.030) and increased ornithine (P = 0.002) were found in the ammonia-removing liver, and after high ammonia (35 mg/m3) exposure, glutamine synthetase (GS) expression was increased (P = 0.012). An increased glutamate (P = 0.004) and decreased glutaminase (GLS) expression (P = 0.083) were observed in the lungs after high ammonia exposure. There was also an increasing trend of glutamine in the kidneys after high ammonia exposure (P = 0.066). For branched-chain amino acid (BCAA) catabolism, high ammonia exposure increased BCAA content in both the lungs and muscle (P < 0.05), whereas below 25 mg/m3 ammonia exposure increased BCAA only in the lungs (P < 0.05). The expression of BCAA transaminase (BCAT1/2) and dehydrogenase complex (BCKDHA/B and DBT) were inhibited to a varying degree in the liver, lungs and muscle after above 25 mg/m3 ammonia exposure, especially high ammonia exposure. The expression of BCKDH complex and glutamate-glutamine metabolism-related genes were highly expressed in the liver, followed by the lungs and muscle (P < 0.01), whereas the BCAT2 expression was highest in the lungs (P = 0.002). Altogether, low ammonia exposure sufficed to evoke the urea cycle to detoxify ammonia in the liver. The process of ammonia removal in the liver and potential ability of the lungs to detoxify ammonia were enhanced with increasing ammonia. Furthermore, high ammonia exposure impaired the BCAA catabolism and decreased the transcripts of the BCAA catabolism-related enzymes, resulting in high BCAA content in extrahepatic tissues. Therefore, with aerial ammonia increasing, an increased urea cycle and glutamine synthesis were ammonia defensive strategies, and high ammonia exposure impaired the BCAA catabolism.
RESUMO
An experiment was conducted to investigate the effects of dietary pantothenic acid levels on growth performance, carcass traits, pantothenic acid status, and antioxidant status of male white Pekin ducks from 15 to 42 D of age and to evaluate the requirement of this vitamin for growing ducks. Different levels pantothenic acid (0, 2, 4, 6, 8, and 10 mg/kg) were supplemented to a corn-soy isolate protein basal diet to produce 6 dietary treatments with different analyzed total pantothenic acid levels (4.52, 6.44, 8.37, 9.88, 12.32, and 14.61 mg/kg). A total of 240 15-day-old male white Pekin ducks were allotted to 6 dietary treatments with 8 replicate pens of 5 birds per pen. At 42 D of age, growth performance, carcass traits, tissue pantothenic acid concentrations, and antioxidant status of white Pekin ducks were examined. Significant effects of dietary pantothenic acid on BW, average daily weight gain (ADG), plasma, and liver pantothenic acid concentrations were observed (P < 0.05) but not carcass traits. The growing ducks fed the basal diet without pantothenic acid supplementation had the lowest BW, ADG, plasma, and liver pantothenic acid content among all ducks (P < 0.05). In addition, the ducks fed the basal diet without pantothenic acid supplementation showed the lowest antioxidant capacity indicated by greatest plasma malondialdehyde content and lowest liver total antioxidant capacity (P < 0.05). And, these criteria responded linearly as dietary pantothenic acid levels increased (P < 0.05). These results indicated that dietary pantothenic acid supplementation improved growth performance and antioxidant status of the growing ducks. In accordance with the broken-line model, the pantothenic acid requirements (based on dietary total pantothenic acid) of male white Pekin ducks from 15 to 42 D of age for BW, ADG, and plasma and liver pantothenic acid contents were 10.18, 10.27, 12.06, and 10.79 mg/kg, respectively.