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Moreno Paolini

Publications and source records attributed to Moreno Paolini.

22 records · Page 2Linked to original sources
PubMed2002

In vitro induction of benzo(a)pyrene cell-transforming activity by the glucosinolate gluconasturtiin found in cruciferous vegetables.

Cytotoxic and cell-transforming activity of gluconasturtiin (GNST), a promising chemopreventive agent commonly found in human diet, was studied in a medium-term bioassay utilizing BALB/c 3T3 cells. We also assessed whether GNST coupled with myrosinase, thus yielding product phenylethyl isothiocyanate (as shown by gas chromatography-mass spectral analysis), can affect the transforming potential of benzo(a)pyrene (B(a)P). Neither cytotoxicity nor cell-transforming activity was recorded. On the contrary, a marked increase (up to sevenfold) of the transforming activity of B(a)P was seen. This cocarcinogenic potential could be ascribed to an imbalance among bioactivation/detoxication during cell growth. These results indicate the need for an overall toxicological characterization of a chemopreventive agent prior to large-scale use.

3T3 Cells↗
PubMed2002

Ursodeoxycholic acid (UDCA) prevents DCA effects on male mouse liver via up-regulation of CYP [correction of CXP] and preservation of BSEP activities.

To investigate whether ursodeoxycholic acid (UDCA) can prevent metabolic impairment induced by deoxycholic acid (DCA), we evaluated the effects of these bile acids on murine CYP enzymes and the relationship with canalicular bile salt export pump (Bsep) expression. In Swiss Albino CD1 mice, UDCA and DCA were injected intraperitoneally either singly, concurrently, or sequentially (UDCA 1 hour before DCA) at equimolar 24.4 mg/kg body weight (BW) doses. CYP content, NADPH-CYP-c-reductase, and individual mixed function oxidases (MFO) were measured 24 hours later. Modulations were observed mainly in males: whereas DCA decreased MFO activities to various isoenzymes with respect to controls (up to 43%, CYP1A2-linked activity), UDCA boosted them (up to 6-fold, testosterone 16 beta-hydroxylase); concurrent administration of UDCA and DCA provided a preventive effect, enhancing MFO activity with respect to single administration of DCA by up to 4.4-fold in the CYP3A1/2 and CYP2B1/2 (6 beta-hydroxylase) and by 2.1-fold in the CYP2E1 (p-nitrophenol hydroxylase). In males (but not females), sequential administration (UDCA then DCA) produced a rather similar protective pattern, but the extent of recovery was generally smaller. Western immunoblotting results for the most affected isoenzymes (CYP3A1/2 and CYP2E1) and Bsep confirmed that UDCA can both prevent and reduce the CYP-dependent MFO inactivation and Bsep down-regulation caused by DCA. These findings may shed further light on the mechanisms responsible for UDCA's protective role in the treatment of cholestatic liver disease.

ATP Binding Cassette Transporter, Subfamily B, Mem↗