Deterioration of muscle quality caused by ammonia exposure in rainbow trout(Oncorhynchus mykiss)

In order to explore deterioration of muscle quality caused by ammonia exposure in rainbow trout(Oncorhynchus mykiss),and then preliminarily investigating the regulatory mechanism of muscle quality in O.mykiss after ammonia exposure based on the lipid metabolism,different concentrations of ammonia stress experiment were conducted,and the physicochemical properties of muscle,antioxidant system,products of energy and lipid metabolism were investigated at total ammonia concentration of 0(control group),10 mg/L(T1),20 mg/L(T2),30 mg/L(T3),45 mg/L(T4)and 60 mg/L(T5).In comparison with the control group,the fillets after ammonia stress exhibited higher a^(*)value,expressible moisture,essential amino acids(EAA),the bitter amino acid and mono-saturated fatty(MUFA),less the umami and sweet amino acids and polyunsaturated fatty acid(PUFA),worse flavor and taste.The lower ammonia exposure(lower than 30 mg/L)did not change the content of EPA and DHA while significant decreases were observed after higher ammonia exposure(higher than 30 mg/L).Meanwhile,the lower ammonia exposure activated the antioxidant system and higher ammonia exposure inactivated antioxidant enzymes to defend against reactive oxygen species(ROS).Moreover,the expression of d9D,FAS,LPL,PPARa,PPARy and SREBP were inhibited and the expression of CPT1 was promoted after ammonia stress,inhibiting lipid synthesis and promoting lipid oxidation.The results are important in estab-lishing the relationship among muscle quality,lipid metabolism and the environmental adaptability of rainbow trout(O.mykiss).

Aerial ammonia exposure induces the perturbation of the interorgan ammonia disposal and branched-chain amino acid catabolism in growing pigs

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/m^(3) ammonia respectively for 25 d.After above 25 mg/m^(3) 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/m^(3))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/m^(3) 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/m^(3) 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.