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S Lerman

Publications and source records attributed to S Lerman.

119 records · Page 7Linked to original sources
PubMedDate not supplied

Ethanol, thyroid hormones and acute liver injury: is there a relationship?

Alcoholic liver disease continues to be an important cause of morbidity and mortality, and the hypermetabolic hypothesis continues to be an attractive area for research. However, the current state of knowledge does not allow unequivocal acceptance or rejection of the role of thyroid hormone and antithyroid medication in alcoholic hepatitis. Clinical trials will help to establish or disprove the veracity of this hypothesis. What has been established is that chronic ethanol ingestion enhances EMR (19-22) which probably reflects the degree of hepatocellular necrosis, at least when relatively mild (25). The influence of thyroid hormone or a hyperthyroid-like state on EMR would be established if it could be shown that different antithyroid medications inhibit the enhanced EMR in chronic alcoholics. This effect has been shown in rats (125), but not in man. It is not apparent that events in the rat model can be readily applied to man. Furthermore, proof that antithyroid medications can inhibit enhanced EMR in chronic ethanol-consuming patients may allow this feature to be used to select patients who may best benefit from such treatment. A controlled randomized clinical trial using different anti-thyroid medications in alcoholic hepatitis may shed light on this important question. At the very least, demonstration of inhibition of enhanced EMR by antithyroid medications may provide the rationale for research concerning the role of thyroid hormone (or a similar hypermetabolic factor) in alcohol-mediated hepatocellular injury.

Alcohol Oxidoreductases↗
PubMedDate not supplied

The metabolism of arsenite and arsenate by the rat.

Differences in distribution and metabolism of arsenite and arsenate were studied in rats and in rat liver and kidney slices and hepatocytes. Five minutes after i.v. administration of 4.8 nmol arsenite or arsenate to male Sprague-Dawley rats, blood levels of arsenic were only 10 percent of the initial dose. Blood arsenic levels then rose: by 4 hours about 67 percent of the initial dose of arsenite and 28 percent of the initial dose of arsenate were in the blood compartment. The predominant form of arsenic in the RBC was dimethylarsinic acid (DMA). Arsenite was rapidly distributed to both liver and kidney; arsenate was rapidly distributed to kidney only. After 4 hours of exposure to arsenite, liver slices had taken up six times more arsenic and kidney slices two times more arsenic than after exposure to arsenate. Isolated hepatocytes took up as much as 20 times more arsenic after arsenite exposure. DMA was found in the medium of the liver slices and hepatocytes exposed to arsenite, but very little DMA was found in the medium of the arsenate-exposed liver slices and hepatocytes. However, five times more DMA was found in the medium of the kidney slices exposed to arsenate than in the medium of the liver slices. Phosphate inhibited uptake and metabolism of arsenate by kidney slices. These studies indicate that inorganic arsenic is rapidly taken up by liver and kidney and methylated. Arsenite is methylated by both organs, whereas arsenate may be methylated by kidney only.

Animals↗
PubMedDate not supplied

Illness and excretion of organophosphate metabolites four months after household pest extermination.

Diethyl phosphate (DEP), an organophosphate metabolite, was found in the urine of symptomatic residents who resided in a household that had been sprayed with diazinon 4.5 mo earlier. Pre- and post-decontamination data with regard to symptoms, DEP, cholinesterase, and surface and air levels underscore the utility of alkyl phosphate metabolites for monitoring exposure. The data also emphasize the efficacy of clean-up measures when baseline data are not available to determine if "within-normal" cholinesterase levels are, in fact, depressed.

Adult↗