Diets containing vegetable tannins, predominantly hydrolysable gallotannins, at levels of 13.5, 25 and 50 g/kg were fed to growing broiler cockerels to examine their effect on enzymes in the pancreas, the intestinal lumen and the intestinal mucosa. Pancreas weight per unit live weight showed a significant (P < 0.05) increase with increasing level of dietary tannin while that of the liver remained unaffected. Trypsin (EC 3 . 4 . 2 1 .4) and a-amylase (EC 3.2.1.1) activities in the pancreas of birds fed at the highest level of tannins were more than double those from birds fed on a tannin-free control diet. In the intestinal lumen inhibition of trypsin activity increased with increasing level of dietary tannin; a-amylase activity was inhibited at intermediate tannin levels but was restored at the highest level. Dipeptidase (EC 3.4.13.11) and sucrose a-glucosidase (disaccharidase) (EC 3.2.1.48) in the intestinal mucosa were both inhibited by tannins. Growth of the birds and digestibility of nitrogen were adversely affected by the tannin-containing diets.Tannin : Pancreatic enzymes : Brush border enzymes : Cockerel It is well established that tannins are potential protein precipitants (Hagerman & Butler, 1980;Hagerman & Klucher, 1986; Makker et al. 1987) and that they reduce the digestibilities of proteins (Mohammed & Ahnied, 1987) when present in animal feeds. Elevated faecal nitrogen excretion associated with ingestion of tannin-containing feeds is ascribed largely to interactions between either tannins and dietary protein or tannins and digestive enzymes, or both. However, Mitjavilla et al. (1977) concluded that the excess faecal N is mostly a result of mucus hypersecretion.Studies in vitro (Griffiths, 1981 ;Lumen & Salamat, 1980;Horigome et al. 1988) and in vivo (Griffiths & Moseley, 1980; Horigome er al. 1988) have demonstrated the formation of tannin-enzyme complexes. However, adopting a technique in vitro more relevant to the situation in vivo, Mole & Waterman (1987) showed that trypsin retained all its activity in the presence of tannic acid when the system included a substrate protein (bovine serum albumin ; BSA) and glycocholic acid, indicating that under such conditions tannins have a preferential affinity for dietary protein over enzyme protein. In previous work Mole & Waterman (1985) had shown that the formation of complexes between tannins and BSA, used as a substrate for proteolysis, could result in either enhancement or inhibition of proteolysis, or no effect at all depending on the tannin:BSA ratio in the complex.In contrast to what had been reported with rats (Griffiths & Moseley, 1980; Horigome et ul. 1988), tannins were shown to exert no effect on protein digestion by insect herbivores (Martin et ul. 1985(Martin et ul. , 1987 in terms of changes in activities of enzymes in the lumen of the small intestine, in order to provide further insight into the mode of action of dietary tannins. A further aim was to examine the effect of dietary tannins on the activity of membrane-bound enzymes wh...

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The antineoplastic nitrosourea CCNU is a known hepatotoxin which has been shown to cause hyperbilirubinemia and reduction in bile flow. We studied morphological alterations in the common bile duct and interlobular bile ducts at 6, 12, and 24 h in male rats given a single oral dose (50 mg/kg) of CCNU. The portal vein was perfused with 1.0% glutaraldehyde fixative. Portal areas and the common bile duct were selectively dissected and processed using standard methods for light and transmission electron microscopy. The epithelial cells of larger common bile duct and interlobular bile ducts showed increased rough endoplasmic reticulum, markedly increased free ribosomes, and mitochondrial degeneration at 6 and 12 h after CCNU. There was also bile imbibition and loss of microvilli, which increased in severity at 12 and 24 h. The interstitium showed infiltration by acute inflammatory cells and dilated capillaries at 6 h. By 24 h, degeneration of epithelial cells was extensive; cells became necrotic and sloughed into the duct lumen. The smaller bile ductules showed no significant degenerative changes; adjacent hepatocytes were unremarkable. Early CCNU injury appears localized in the large bile ducts and reflects inflammatory edema, bile stasis, and degeneration of epithelial cells. Our studies suggest that this ductal injury may reflect metabolism of CCNU to reactive species within the bile ducts.

Using the micronucleus test we have found no significant difference between germ-free and conventional (non-germ-free) male CD-1 mice gavaged twice with 440 or 880 mg benzene/kg. Hence, the higher myeloclastogenicity observed previously with the p.o. (4-6 times) than with the i.p. route of benzene administration was ruled out as being due to the involvement of gut flora in benzene biotransformation. Pretreatment of males with 3-methylcholanthrene or beta-naphthoflavone, inducers of P-448 monooxygenase, but not phenobarbital, an inducer of P-450, significantly enhanced the myeloclastogenic effect of a single oral dose of benzene (440 mg/kg). Single oral doses of phenol, catechol, or hydroquinone (250, 150, and 200 mg/kg, respectively) failed to reproduce the potent myeloclastogenic effect of benzene. In fact, only hydroquinone was mildly clastogenic. The relation between benzene's myeloclastogenicity and metabolism is discussed.