Search PubMed⌕ Search

Biomedical subjects

S Schenker

Publications and source records attributed to S Schenker.

At least 199 records · Page 11Linked to original sources
PubMed1975

Reversible impairment of cerebral DNA synthesis in thiamine deficiency.

The effect of thiamine deficiency on rat brain DNA and RNA synthesis was investigated. Thiamine deficiency, culminating in encephalopathy (symptomatic stage) was induced by dietary thiamine deprivation of 4 to 5 weeks. The encephalopathy could be completely reversed within 6 hours by paranteral administration of thiamine. Controls consisted of pair-fed and ad libitum-fed littermates given the same diet supplemented with thiamine. Brain DNA and RNA synthesis was determined by administration of labeled thymidine, orotic acid, or adenine into the cerebral ventricle and measuring the incorporation of the appropiate labeled precursor into DNA or RNA. Thiamine deficiency(symptomatic stage) had no effect on net DNA and RNA level in any brain area studied. Also, no consistent alteration of brain RNA synthesis was shown in severe thiamine seficiency. By contrast, DNA synthesis in symptomatic thiamine-deficient ratswas reduced to 22, 37, 31, and 19 percent, respectively; of pair-fed control values in the cortex, brain stem, cerebellum, and subcortical structures (p less than 0.05). Thedegree of depressed DNA synthesis increased with the extent and duration of thiaminedeprivation. Following reversal of the encephalopathy with parenteral thiamine, DNAsynthesis in all brain areas increased markedly to and above control values. Thses data indicate that the thiamine deficiency state interferes with the synthesis ofsome discrete DNA pool(s) in the brain. This effect may be due to thiamine deficiency per se and /or some thiamine-induced impaired food assimilation or utilization.

Adenine↗
PubMed1975

Fatty liver induced by tetracycline in the rat. Dose-response relationships and effect of sex.

Dose-response relationships, biochemical mechanisms, and sex differences in the experimental fatty liver induced by tetracycline were studied in the intact rat and with the isolated perfused rat liver in vitro. In the intact male and female rat, no direct relationship was observed between dose of tetracycline and hepatic accumulation of triglyceride. With provision of adequate oleic acid as a substrate for the isolated perfused liver, a direct relationship was observed between dose of tetracycline and both accumulation of triglyceride in the liver and depression of output of triglyceride by livers from male and female rats. Marked differences were observed between female and male rats with regard to base line (control) hepatic concentration of triglyceride and output of triglyceride. Accumulation of hepatic triglyceride, as a per cent of control values, in response to graded doses of tetracycline, did not differ significantly between male, female and pregnant rat livers. However, livers from female, and especially pregnant female rats, were strikingly resistant to the effects of tetracycline on depression of output of triglyceride under these experimental conditions. These differences between the sexes could not be related to altered disposition of tetracycline or altered uptake of oleic acid. Depressed hepatic secretion of triglyceride accounted only for 30 to 50% of accumulated hepatic triglyceride, indicating that additional mechanisms must be involved in the production of the triglyceride-rich fatty liver in response to tetracycline.

Animals↗
PubMed1975

Thiamine transport across the rat intestine. II. Effect of ethanol.

We have previously investigated the normal characteristics of thiamine intestinal transport in rats and found that a very low concentrations (0.06 to 2.0 muM) thiamine transport is a saturable, carrier-mediated, active process while at high concentrations (greater than 2.0 muM) transport proceeds by simple diffusion. The present studies were undertaken to characterize the effect of ethanol on thiamine transport. Intact isolated loops were used to measure rates of 35S-thiamine hydrochloride absorption into the circulation in vivo, and everted jejunal segments to measure net transmural flux, unidirectional uptake, and cellular exit of 14C-thiamine hydrochloride in vitro. Intragastric administration of ethanol (50 to 750 mg. per 100 grams of weight) reduced absorption of low thiamine concentration in vivo to 65.44 per cent of control value. A similar inhibition was noted after intravenous ethanol. Once attained, the inhibition of thiamine absorption was not related to the ethanol dose or to ethanol concentration in the blood or in the intestinal lumen; this inhibition was reversible. In contrast, ethanol did not affect absorption of high concentrations of thiamine. These findings were confirmed by the in vitro results. In transmural flux studies, the movement of low, but not high, thiamine concentration against a concentration gradient was inhibited by ethanol, so that the normal serosal/mucosal ratio of 1.5 was reduced to 1.0. Ethanol did not affect unidirectional uptake into the mucosa of either low or high thiamine concentrations, but blocked cellular exit of low thiamine concentrations from the cells into the serosal compartment. Exit of high thiamine concentrations was not affected. Ouabain, like ethanol, markedly reduced cellular exit but did not influence uptake of low thiamine concentrations. The present studies suggest that ethanol adversely affects the active, but not the passive, component of thiamine transport. Moreover, ethanol appears to block thiamine exit from the cells but does not affect cellular uptake of thiamine. The similarity to ouabain action suggests that ethanol may impair active thiamine transport by inhibiting Na-K ATPase activity.

Animals↗
PubMed1975

The effect of liver disease in man on the disposition of phenobarbital.

The disposition of phenobarbital (PB) was studied in normal individuals and in patients with cirrhosis or acute viral hepatitis to determine 1) if there is significant impairment of PB metabolism in hepatic disease and 2) to what extent such abnormal disposition of the drug affects its disappearance from blood. The diagnosis of liver disease was based on characteristic clinical findings, biochemical liver "function" tests and liver biopsy when necessary. All individuals had normal renal function and were free of other drug and alcohol intake for at least 3 weeks. With radiotracer methodology, PB and its principal metabolites, p-hydroxyphenobarbital (PBOH) and conjugated PBOH (PBOC), were monitored in blood and urine for 5 days after a single dose of 14-C-PBadministered intraduodenally. PB blood half-life (T1/2) in the control group was 86 plus or minus 3 hours (S.E.). In cirrhotics the T1/2 was prolonged to 130 plus or minus 15 hours (P less than .001) and this was accompanied by a 50% reduction in urinary PBOC excretion (P less than .05). Urinary excretion of PB and PBOH was unaltered by cirrhosis. In patients with acute viral hepatitis, PB T1/2 was not significantly prolonged and urinary excretion of PB and its metabolites was in the normal range (P greater than .05). No PBOH and only traces of PBOC were detected in the blood of either control individuals or patients with liver disease. Urinary excretion of unchanged PB was an important elimination pathway of the drug in all groups. As a result of this, PB T1/2 in cirrhosis was only moderately prolonged.

Adult↗