Co/Ba/La2O3 catalyst for ammonia synthesis under mild reaction conditions

Ruthenium catalysts may allow realization of renewable energy–based ammonia synthesis processes using mild reaction conditions (<400 °C, <10 MPa). However, ruthenium is relatively rare and therefore expensive. Here, we report a Co nanoparticle catalyst loaded on a basic Ba/La2O3 support and pre-reduced at 700 °C (Co/Ba/La2O3_700red) that showed higher ammonia synthesis activity at 350 °C and 1.0–3.0 MPa than two benchmark Ru catalysts, Cs+/Ru/MgO and Ru/CeO2. The synthesis rate of the catalyst at 350 °C and 1.0 MPa (19.3 mmol h−1g−1) was 8.0 times that of Co/Ba/La2O3_500red and 6.9 times that of Co/La2O3_700red. The catalyst showed activity at temperatures down to 200 °C. High-temperature reduction induced formation of a BaO-La2O3 nano-fraction around the Co nanoparticles, which increased turnover frequency, inhibited Co nanoparticle sintering, and suppressed ammonia poisoning. These strategies may also be appliable to nickel catalysts.

Ammonia Toxicity Induces Oxidative Stress, Inflammatory Response and Apoptosis in Hybrid Grouper (♀ Epinephelus fuscoguttatus × ♂ E. lanceolatu)

To study the effects of acute ammonia stress on the poisoning reaction of the hybrid grouper (♀ Epinephelus fuscoguttatus × ♂ E. lanceolatu), 300 healthy grouper juveniles with an initial body weight of 51.4 ± 2.57 g were selected for an acute ammonia stress experiment using a half-lethal concentration of ammonia for 24, 48, 72, and 96 h with triplicate. The results show that (1) The half-lethal concentrations of ammonia for a hybrid grouper were 39.5 mg/L for 24 h, 27.3 mg/L for 48 h, 26.5 mg/L for 72 h, and 25.0 mg/L for 96 h, and the safe concentration was 2.50 mg/L. (2) The biochemical indices of the serum and livers of the groupers fluctuated under acute ammonia stress (P &lt; 0.05), and the contents of serum cortisol and lactate reached the maximum value in 72 h (P &lt; 0.05). (3) 24 h ammonia stress increased the activities of alkaline phosphatase, acid phosphatase, catalase, glutathione peroxidase, superoxide dismutase, lysozyme, and the content of immunoglobulin M in the liver (P &lt; 0.05). Meanwhile, all ammonia-stressed fish groups had an increased amount of malondialdehyde in the liver (P &lt; 0.05). (4) The ammonia poisoning caused significantly up-regulation of antioxidant genes, inflammatory cytokines, and apoptosis genes (P &lt; 0.05), and the expression of inflammatory cytokines and apoptosis genes were the highest in 24 h ammonia stress group. (5) The ammonia content in the water changed the abundance and evenness of intestinal microbes in grouper, mainly in that ammonia stress significantly increased the relative abundance of fusobacteria, but significantly decreased the relative abundance of gemmatimonadetes (P &lt; 0.05). It was speculated that apoptosis induced by ammonia poisoning in grouper may be related to oxidative stress and the activation of inflammatory factors, and excessive inflammatory stress may be one of the causes of ammonia poisoning in the hybrid grouper.

Ammonia poisoning causes muscular but not liver damage in cattle

Twelve steers were intraruminally administered a high dose (0.5g/kg BW) of urea to study the damage effect of ammonia poisoning on liver and/or muscles. Blood samples were collected to determine ammonia and activities of gammaGT, AST and CK. Eleven steers were successfully poisoned and treated properly, but one succumbed. Poisoned cattle showed high concentration of ammonia, and higher activities of AST and CK. The higher the ammonia, the greater were the activities of AST (r=0.59) and CK (r=0.61). The correlation between AST and CK was high and significant (r=0.80), but not between AST and gammaGT (r=0.19). The activities of AST and CK were higher after the beginning of the convulsive episodes due to ammonia poisoning. Those results showed that occurred muscle damage instead of liver damage since CK is a typical enzyme from skeletal muscle; AST is found either in skeletal muscle and hepatocytes, while gammaGT is present in hepatic cells.

An Outbreak of Ammonia Poisoning from Chicken Tenders Served in a School Lunch

Although foodborne outbreaks of illness are relatively common, they are rarely caused by chemical agents. An outbreak of gastrointestinal illness occurred among students at two schools shortly after lunch was served. A cohort study, an environmental investigation, and microbiological and toxicological laboratory testing of food samples were performed. A case was defined as a student or teacher who ate food prepared in the kitchen at school A on 25 November 2002 (and served at schools A and B) and who later developed headache or symptoms of gastrointestinal tract irritation, with onset within 180 min of eating lunch. Among 312 persons interviewed, 157 persons became ill (attack rate = 49%; attack rate 41% for school A, 11% for school B). Onset of illness occurred within 60 min for 81% of cases; 91% of students reported that their chicken tenders smelled unusual. Eating chicken tenders that smelled unusual was associated with being a case (relative risk 9.2, 95% confidence interval 1.4 to 62.6, P &lt; 0.05). Ammonia was detected in uncooked chicken tenders at levels as high as 2,468 ppm. The chicken had been contaminated during a warehouse leak of ammonia refrigerant. This outbreak of ammonia poisoning is only the second reported in food, and the first in a solid food. Heated chicken tenders contaminated with ammonia can cause acute illness within a short period of time.