Activity and structure of stored aerobic granules.

This study investigates how storage temperatures and periods under extended idle conditions affected the stability and activity of granules that have a high phenol-degrading capability. The granule activity increased as storage temperature decreased, and declined as storage time increased. Granules stored with pure water at room temperature (20.8+/-5.6 degrees C) lost stability after three months storage. Particularly, granules stored with 500 mg l(-1) phenol solution demonstrated high phenol degradation capability following storage. Further, storage at subfreezing temperatures (-20 degrees C) is an ideal way of preserving stability and activity of phenol-fed granules. Anaerobic degradation of proteins in granule core by obligate anaerobic strain such as Bacteroides sp. corresponded to the stability loss of stored granules.

Effects of aflatoxin B1 on the hepatic microsomal mixed function oxidase system during phenobarbital and benzo(a)pyrene treatment in chickens.

Administration of 1.5 mg aflatoxin B1 (AFB1)/kg in DMSO as a single i.p. dose to 80 mg phenobarbital/kg i.p. for 3 d pretreated chickens showed significant decrease in the levels of electron transport components and drug metabolizing enzymes compared to phenobarbital administration alone. Induction of mixed function oxidase enzymes due to phenobarbital was not affected by the AFB1 pretreatment. AFB1 administration to 20 mg benzo(a)pyrene/kg in safflower seed oil i.p. for 2 d pretreated chickens showed significant decrease in cytochrome b5 and drug metabolizing enzymes when compared with benzo(a)pyrene treatment alone. However, cytochrome P450 level was slightly higher due to administration of AFB1 to benzo(a)pyrene-injected chickens. The results indicate that the phenobarbital-induced cytochrome P450 is more susceptible to AFB1 than benzo(a)pyrene-induced cytochrome P450.

Effects of aflatoxin B1 on liver microsomal enzymes in different strains of chickens.

Administration of Aflatoxin B1 (AFB1) with safflower seed oil to hubbard chickens caused a significant increase in liver microsomal protein, electron transport components, and drug metabolizing enzymes. No alteration was observed in the activity of alanine and aspartate aminotransferases. AFB1 treatment with dimethylsulfoxide (DMSO) as a vehicle caused a significant decrease in electron transport components, drug metabolizing enzymes, and a significant increase in the activity of aspartate aminotransferase. Higher inhibition was observed at 1.5 mg/kg dose level of AFB1. Inhibition by AFB1 was maximal after 24 hr of treatment and decreased thereafter. AFB1 treatment with DMSO caused no significant change in electron transport components and drug metabolizing enzymes in Rhode Red Island (RRI) strain. Vancob male chickens showed significant decrease in electron transport components and drug metabolizing enzymes, while a significant increase was observed in vancob females. Results suggest that the effects of AFB1 depend on treatment vehicle, strain and sex of chickens.

Effect of sulfamethazine on phenobarbital and benzo[a]pyrene induced hepatic microsomal mixed function oxidase system in rats.

Administration of sulfamethazine (300 mg/kg, i.p., single dose) to phenobarbital (80 mg/kg, i.p., 3 days) pretreated rats showed significant decrease in microsomal protein, electron transport components and drug metabolizing enzyme activities, compared with phenobarbital administration alone. Induction of mixed function oxidase enzymes due to phenobarbital was not affected by the pretreatment of sulfamethazine. Sulfamethazine administration to benzo[a]pyrene (20 mg/kg, i.p., 2 days in oil) pretreated rats showed no significant change, but there was a slight decrease in cytochrome P450 and aminopyrine N-demethylase activity, compared with benzo[a]pyrene administration alone. A significant inhibition was observed in aminopyrine N-demethylase activity due to in vitro addition of sulfamethazine (3.5 mM) to microsomal incubations from untreated, sulfamethazine, phenobarbital and benzo[a]pyrene-treated rats. The results indicate that the phenobarbital induced cytochrome P450 is more susceptible to sulfamethazine than benzo[a]pyrene induced cytochrome P450.