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P Schroth

Publications and source records attributed to P Schroth.

4 recordsLinked to original sources
PubMed1992

1-C-glucuronidation of N-nitrosodiethylamine and N-nitrosomethyl-n-pentylamine in vivo and in primary hepatocytes from rats pretreated with inducers.

The organ specificity of the carcinogenic action of nitrosamines is partly explained by organ specific activation. The specificity might also be determined by conjugation of reactive intermediates in e.g. the liver. 14C-Labeled N-nitrosodiethylamine (NDEA) a liver carcinogen and N-nitrosomethyl-n-pentylamine (NMPentA) which induces esophageal and nasal tumors were administered to rats or incubated with primary cells. Urine and cell extracts were separated by HPLC after addition of synthetic marker glucuronides and these were quantified by liquid scintillation counting. In urine of rats treated with NDEA 0.03% of administered nitrosamine was recovered as the O-glucuronide derived from N-nitroso-1-hydroxyethylethylamine. In rats treated with NMPentA 2.86% was metabolized to the glucuronide at the methyl group. In hepatocytes of untreated rats 0.03% of the added NDEA was conjugated to the glucuronide, phenobarbital pretreatment induced this conjugation reaction 5-fold. Hepatocytes from untreated rats metabolized 1.2% of NMPentA to the primary glucuronide; after phenobarbital pretreatment this value increased to 1.6%. In hepatocytes from 3-methylcholanthrene-pretreated rats, 0.04% of NMPentA was metabolized to the glucuronide derived from N-nitroso-1-hydroxy-n-pentyl-methylamine, while 0.85% was derived from N-nitroso-hydroxymethyl-n-pentylamine. In hepatocytes from Aroclor-pretreated rats, 0.09% were pentyl conjugates and 1.1% methyl conjugates. The induction pattern and organ specificity of glucuronidation indicate that all three 1-hydroxy nitrosamines are conjugated by group II phenobarbital inducible UDP-glucuronosyltransferase activity. The lipophilicity of a nitrosamine seems to determine the extent of glucuronidation in hepatocytes and in vivo. No glucuronides derived from either NDEA or NMPentA were detectable in incubations with kidney cells, nor was the glucuronide of NDEA found in incubations with whole bladders.

Animals↗
PubMed1991

Dietary restriction on serum thyroid hormone levels.

To determine the long term effects of a protein sparing fast on serum thyroid hormone levels, the authors studied 38 obese patients ingesting a diet of 320 kcal for up to 13 weeks. The high baseline serum triiodothyronine (T3) levels decreased significantly by the first week, further decreased by the third week, and this lower level persisted for the duration of the fast until realimentation. Serum free T3 index followed the same general pattern as did serum T3 levels. Serum reverse T3 increased significantly by the first week, but by week three, the reverse T3 level had begun to fall, although still significantly increased above baseline. By week seven, reverse T3 had decreased to almost baseline and remained not significantly changed from the baseline to 13 weeks. Serum thyroxine (T4) increased significantly by the first week in all patients, but by the third week had returned to baseline levels which persisted to 13 weeks. The free T4 index and free T4 concentrations showed the same increment at week one and then returned to baseline levels. There were no significant changes in serum thyroxine-binding globulin (TBG) or thyroid-stimulating hormone (TSH) concentrations. The changes in serum T3 and reverse T3 levels are attributable to alterations in peripheral 5'-monodeiodination of T4 and reverse T3 induced by the protein sparing fast.

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