http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=6425817 1: Poult Sci. 1984 Mar;63(3):485-91. Experimental induction of chronic aflatoxicosis in chickens by purified aflatoxin B1 and its reversal by activated charcoal, phenobarbital, and reduced glutathione Dalvi RR, McGowan C. Aflatoxin B1 (AFB1) caused dose-dependent reductions in weight gain and feed consumption when day-old Hubbard X Hubbard broiler type chicks were maintained on a diet contaminated with either 0, 2.5, 5, or 10 ppm purified AFB1 for 8 weeks. Although changes in these parameters were detected at the 2.5 and 5 ppm, the most profound changes were evident at 10 ppm contamination. The concentration of cytochrome P-450 in hepatic microsomes, measured at the end of 8 weeks, also showed dose-dependent decreases. Cytochrome P-450 content in chickens receiving 2.5, 5, and 10 ppm AFB1 was 16, 28, and 65%, respectively, less than the control. Microsomal benzphetamine N-demethylase activity was not inhibited by 2.5 or 5 ppm, but ingestion of 10 ppm AFB1 reduced its activity by more than 40%. Serum glutamic oxalacetic transaminase (SGOT) levels of chickens receiving 10 ppm AFB1 increased by more than 100%, indicating substantial liver damage. However, birds simultaneously receiving 10 ppm AFB1 and activated charcoal (.1% in the feed) or either reduced glutathione (.05%) or phenobarbital (.05%, given intermittently) in their drinking water showed a trend of improvement in feed consumption (less than 10% reversal) and weight gain (less than 28% reversal) over the birds receiving 10 ppm AFB1 alone. The results also indicate that the simultaneous presence of these agents with AFB1 considerably prevented the inhibitory effect of AFB1 on the microsomal cytochrome P-450 and benzphetamine N-demethylase activity. Furthermore, these agents were able to provide moderate protection against AFB1-induced liver injury manifested by elevation of SGOT activity.