Intestinal UDPGA concentrations appeared to have a larger range than in liver (65-

258 C1M). The decreased UDPGA concentrations (relative to liver) are reflected in the

decreased UDPGA Km of 27 CIM reported for 4'-OHCB-69 (Table 4-1). The UGT

isoforms in the intestine responsible for OH-PCB glucuronidation operate in a cellular

environment with decreased UDPGA concentrations and thus appear to work optimally at

lower concentrations of co-substrate.

 The physiological hepatic levels of UDPGA are about 4 times lower than the 1.5

mM co-substrate concentrations utilized in the OH-PCB glucuronidation study in catfish

(Chapter 4). In contrast, the physiological intestinal levels of UDPGA are around the

same concentration as the amount used in the UGT assay (200 CIM). This means that the

Vmax reported for hepatic OH-PCB glucuronidation in Chapter 4, probably represent

overestimates that would not be achievable in vivo.

 Conclusions and Recommendations

 A method to directly determine UDPGA in tissue by anion-exchange

chromatography was developed and used to study UDPGA concentrations in channel

catfish liver and intestine. The method was sensitive, reproducible and displayed good

resolution for UDPGA. The technique may be adapted to study other nucleotide sugars.

The hepatic UDPGA levels determined by this technique were similar to those in other

mammalian species and higher than two other fish species. This was the first time

intestinal UDPGA concentrations in any piscine species were determined; the values

were similar to rat, but significantly higher than in human small intestine.

 Future studies should determine the UDPGA concentrations in a greater number of

catfish, as well as in different tissues, including determination of the UDPGA