Experimental induction of chronic aflatoxicosis in chickens
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
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.