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Biomedical subjects

F S Messiha

Publications and source records attributed to F S Messiha.

At least 55 records · Page 3Linked to original sources
PubMed1989

Effect of leucine enkephalin on ethanol produced behavioral depression in the mouse.

The effect of leucine enkephalin (LNK) on spontaneous locomotor activity was studied in mice of both sexes. The effect of a depressant dose of ethanol (ET) on LNK-mediated response on motility was also studied. In addition, the determination of specific activities of the hepatic enzymes primarily involved in the metabolism of ET and acetaldehyde was studied. Lactate dehydrogenase (LDH) isoenzymes were also assayed in both plasma and heart tissues. Intraperitoneal injection of LNK, 100 mg/kg, exerted behavioral depression in the male but not female mouse compared to controls. This effect was apparent for the initial 30 min posttreatment. Injection of two smaller doses of LNK, which were devoid of effect on mouse motility, prior to a depressant dose of ET counteracted ET-caused depression of motility only in the female mouse. This became apparent 30 min postdrug injection and lasted for 60 min thereafter. The LNK and ET treatment inhibited only male mouse liver aldehyde dehydrogenase in both cytoplasmic and mitochondrial preparations concomitant with reduction of plasma but not heart LDH1 isoenzyme from corresponding controls. The results suggest that LNK and ET affect different systems involved in behavioral depression tested and show a potential for LNK in antagonizing the ET effect studied. The data also indicate a sex-dependent effect of LNK on motility and of its interaction with ethanol on the enzymes studied.

Aldehyde Dehydrogenase↗
PubMed1989

Beta-endorphin-like immunoreactivity levels in the hypothalamus, the periaqueductal grey and the pituitary of the DBA mouse: determination by ELISA and relationship to nociception.

The present paper describes the development and application of an enzyme-linked immunosorbent assay (ELISA) for the assessment of beta-endorphin-like immunoreactivity (beta-ELIR) level in the hypothalamus, the periaqueductal grey (PAG) and the pituitary of DBA/2 mice that were subjected to mild social stress (aggressive confrontation). After confrontation these subjects showed elevated tail-flick latencies (TFL) when compared to controls, a finding that indicates stress-induced analgesia (SIA). A positive correlation was found between individual TFLs and beta-ELIR levels in the PAG but not in the hypothalamus and the pituitary. These results suggest that individual baseline PAG beta-ELIR levels may be taken as a predictor of high degrees of stress-induced analgesia.

Agonistic Behavior↗
PubMed1989

Enkephalins, their constituents and voluntary drinking of ethanol by the rat.

The relationship between the neuropeptides leu-enkephalin, met-enkephalin, kentsin (a contraceptive tetrapeptide) and ethanol was studied in the male rat. This was pursued by assessing the effect of these peptides and some of their amino acid constituents on voluntary drinking of ethanol by rats with preference to alcohol intake. The in vitro effect of some of kentsin amino acids constituents on rat liver alcohol and aldehyde dehydrogenase was also studied. Intraperitoneal injection of leu-enkephalin, but not met-enkephalin, produced a delayed increase in voluntary ethanol drinking by the rat. Injection of identical doses of kentsin produced a much lesser effect than the leu-enkephalin treatment. The separate or combined treatment with phenylalanine and leucine, resulted in decreased voluntary consumption of ethanol. Coadministration of glycine or tyrosine alone or both combined did not influence ethanol drinking. Coadministration of tyrosine or glycine with leucine negated the leucine effect on ethanol drinking. Both L-arginine and L-proline, the two amino acids component of kentsin, decreased the specific activity of rat liver mitochondrial aldehyde dehydrogenase in vitro at 10(-3) mol concentration. The results suggest an interrelationship between the peptides studied and ethanol preference. The data also indicates that some of kentsin action on ethanol drinking may be related to the effect of some of its degradation product on hepatic ethanol-derived acetaldehyde metabolism and/or may be related to the endocrine property of kentsin.

Alcohol Dehydrogenase↗
PubMed1989

A toxicology evaluation of postnatal maternal exposure to cesium.

The effect of postnatal maternal exposure to CsCl on the newborn was studied in the mouse. Maternal ingestion of 1 mEq CsCl solution as the only drinking fluid began immediately after birth and the offspring were breast-fed until weaning. They were then separated from the nursing dams and remained Cs free for a subsequent 2 weeks prior to sacrifice. Maternal Cs exposure decreased the weanling body weight from controls and they attained normal body weight after 2 weeks of Cs-free period during development. Maternal Cs ingestion caused a reduction in offspring brain weight of both sexes compared to controls. The kidney weight of the developing female, but not male, offspring was also decreased from controls as a consequence of maternal Cs exposure. The offspring's hepatic alcohol and aldehyde dehydrogenase were not altered from controls as a function of maternal exposure to Cs salt. Little changes occurred in offspring heart lactate dehydrogenase by the maternal Cs treatment. The results suggest that maternal Cs exposure during breast-feeding affected body weight and the CNS of the offspring. The change noted in weanling kidney weight was sex dependent. These gross pathological changes in weanling organ weight were not apparent when maternal breast-feeding was eliminated. The data indicates that Cs adversely affected the newborn which was eliminated after cessation of the Cs exposure.

Alcohol Dehydrogenase↗
PubMed1989

Maternally-mediated neonatal lithium-cesium interaction in the mouse.

The effect of maternal exposure to LiCl, CsCl or both salts in the weaning and developing offspring mice was studied on selected organ weights, hepatic and cardiac dehydrogenase enzymes. The concentration of alkali metal used in maternal drinking fluid during pregnancy and breast-feeding did not produce taste aversion and therefore approximate equal consumption was assured. Maternal exposure to either alkali metal reduced brain and testis weights of the developing offspring mice compared to controls. This suggests a delayed toxic effect on the CNS and endocrine organs. Coadministration of both salts negated this effect. The maternal neonatal Li-mediated increases of weanling spleen weight and the reduction of testis weight of developing offspring mice by Li or Cs were not evident when both alkali metals were given in combination. The combined maternal exposure to both Li and Cs salts also negated the induction of offspring mouse liver alcohol dehydrogenase produced by either alkali metal alone. Likewise, the induction of developing mouse heart lactate dehydrogenase isoenzyme (LDH5) by maternal exposure to LiCl was no more apparent by the combined Li and Cs treatment. These data suggest a Li+-Cs+ interaction in the offspring mouse due to maternal exposure to these alkali metals during pregnancy and breast-feeding periods. The results also suggest that both alkali metals most probably have been delivered to the suckling pups and some of their toxic effect was retarded.

Alcohol Dehydrogenase↗
PubMed1987

Differential response of NADP-linked hepatic aldehyde dehydrogenase toward taurine: implication for behavioural effects of ethanol.

The effects of taurine, its initial precursor L-cysteine, and the major metabolite taurocholic acid on two ethanol-mediated responses in rodents were studied. Administration of a single dose of taurocholic acid reduced voluntary intake of a 5% ethanol solution by the rat. In the mouse, taurine had no effect on alcohol drinking or on the central depressant action of ethanol, as measured by the duration of ET-produced loss of the righting reflex. Likewise, taurocholic acid and L-cysteine did not significantly influence the duration of ethanol-narcosis time from control mice. Also studied were the effects of acute and short-term (7 or 10 days) administration of these compounds on hepatic ethanol and acetaldehyde metabolizing enzymes. Short-term administration of an equimolar concentration of taurine enhanced endogenous NADP-linked rat liver aldehyde dehydrogenase (L-ALDH) as contrasted with inhibition of the same enzyme by L-cysteine. Short-term (7 days) treatment with L-cysteine induced rat liver NAD-linked ALDH, but acute (single dose) treatment did not. Taurocholic acid short-term administration caused an induction and an inhibition of endogenous mouse liver alcohol dehydrogenase (L-ADH) and L-ALDH, respectively. The results suggest that taurine does not directly interact with ethanol. However, its major metabolite, taurocholic acid, may cause rapid metabolic conversion of ethanol to acetaldehyde by induction of L-ADH, which is then slowly metabolized due to a concomitant inhibition of L-ALDH. This may cause a build-up of acetaldehyde and thereby produce adverse reactions similar to those resulting from the combination of disulfiram and ethanol.

Aldehyde Dehydrogenase↗
PubMed1987

Cerebral distribution of beta-lipotropin and beta-endorphin in infantile progressive spinal muscular atrophy of Werdnig and Hoffman disease.

The regional distribution's profile of beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) was determined in the brain of an infant who died from Werdnig-Hoffmann's disease. Regional levels of beta-endorphin-like immunoreactivity (beta-ELIR), resulting from beta-EP and beta-LPH, were generally low in comparison to the homologous levels found in victims dying of other diseases.

Brain Chemistry↗
PubMed1986

Effect of pre and postnatal lithium chloride ingestion on the developing mouse.

The effect of pre and postnatal maternal ingestion of 1 mEq LiCl, given ad libitum in drinking water, on neonatal development was studied in the mouse. The measurements made included evaluation of body and selected organ weights of the weaning offspring. In addition, determination of weaning mouse liver alcohol dehydrogenase (L-ADH), aldehyde dehydrogenase (L-ALDH) were performed to assess the sensitivity of the offspring to ethanol intoxication due to the clinical trials of lithium salts in alcoholism. Heart lactate dehydrogenase isoenzymes were also assayed to assess developmental aspects of the offspring. Little changes occurred in body weight and only moderate increase in spleen weight was noted without concomitant changes in brain, kidney or liver weight of the nursing dams. Maternal Li+ exposure resulted in increased kidney, liver and spleen but not brain weights from controls in the weaning animals. This effect was greater in the female than in the male offspring. The weaning mice showed an induction of L-ALDH as a consequence of maternal Li-treatment. No changes occurred in the other hepatic and cardiac enzymes studied. The results suggest sex-dependent neonatal sensitivity towards maternal ingestion of a small concentration of LiCl in drinking fluid. Hepatic changes of L-ALDH may represent an early expression of hepatic toxicity in the weaning mouse.

Alcohol Dehydrogenase↗
PubMed1984

Biochemical aspects of cesium administration in tumor-bearing mice.

The effect of pretreatment with CsCl on mice bearing sarcoma I implants was studied as a function of duration of treatment period, life span and tissue Cs+ and K+ levels. Treatment with CsCl for 14 consecutive days prior to sarcoma implantation resulted in initial reduction of the tumor-mediated mortality compared to controls and to a one week pretreatment period with identical doses of CsCl. A large accumulation of endogenous K+ was noted in tumor mass compared to nonmalignant tissue of the same animals or to tumor-free controls receiving identical Cs-treatment. The entry of exogenously administered Cs+ into malignant tissue was less than that accumulating in respective controls. The accumulation of Cs+ in tumor mass was dose-dependent. The ratio of K+:C+ was greater in tumor tissue than in nonmalignant tissue. The results suggest that a critical balance between these alkali metals may be required for adequate Cs effect against the tumor studied.

Animals↗
PubMed1984

Effect of cesium and potassium salts on survival of rats bearing Novikoff hepatoma.

The effect of CsCl on the life span of female Sprague-Dawley rats innoculated with Novikoff's hepatoma was studied as a function of both pre- and post-treatment with CsCl and as a function of the inoculant dose. The effect of KCl on the CsCl treatment was also studied. Rats treated with CsCl for 12 consecutive days prior to or immediately after inoculation with 1.0 ml of viable hepatoma cell suspension showed an increase in mortality score from corresponding controls. Conversely, increases in the dose of the inoculant resulted in delaying the onset of toxicity in rats receiving the Cs-treatment after inoculation as evidenced by a decrease in mortality. Availability of KCl in drinking water ad lib further decreased total mortality when given alone but not when combined with CsCl. The results indicate a dose-dependent paradoxical effect of CsCl on Novikoff hepatoma cell toxicity and suggest a critical intercellular balance requirement between Cs+ and K+ on the effect studied.

Animals↗
PubMed1984

Effect of cesium and ethanol on tumor bearing rats.

The effect of separate and combined administration of 15% ethanol and 0.2% CsCl solution on life span of rats with Novikoff hepatoma implants was studied as a function of time of initiation of treatment. Pretreatment with CsCl alone or combined with ethanol resulted in earlier onset on morbidity compared to the ethanol-treatment or to controls. As high as 87.5% of Cs-treated animals died 16 days post tumor implantation compared to 33% of rats receiving CsCl and ethanol combined. This protective action of ethanol against Cs-evoked toxicity in tumor-bearing rats persisted through the experiment. Animals subjected to drug treatment immediately after tumor transplantation displayed delayed onset of morbidity compared to drug pretreated rats. In both cases the Cs-treatment enhanced morbidity by approximately 2 folds from corresponding controls. Animals sacrificed 18 days post tumor inoculation showed an induction of hepatic alcohol dehydrogenase and an increase in Vmax without changes in the apparent Km by the Cs-treatment. There was an increase in liver mitochondrial aldehyde dehydrogenase of hepatoma-bearing rats from tumor-free controls which was associated with an increase in the apparent Km value. The results indicate potentiation of the hepatoma toxicity by CsCl which may be minimized by ethanol. A role for hepatic enzymes determined in the pathogenesis of tumor line studied and/or their use as a biochemical correlate is suggested.

Alcohol Dehydrogenase↗
PubMed1984

Lithium, rubidium and cesium: cerebral pharmacokinetics and alcohol interactions.

The distribution of exogenously administered Li+, Rb+ and Cs+ in distinct mouse brain regions was studied as a function of time subsequent termination of a short-term daily treatment with these alkali metal salts. The resulting distribution profiles were compared with that obtained from the corresponding endogenous alkali metals. Endogenous Rb+ and Cs+ were readily measurable in all 6 brain regions studied compared to traces of measurable Li+. The Rb+ concentration was greater than that of Cs+. Short-term treatment with equal doses of the alkali metals studied showed greater brain accumulation of Rb+ and Cs+ than Li+ with a prolonged brain regions preference for Cs+ storages as a function of time. Duration of ethanol-mediated narcosis was reduced from saline controls by pretreatment with RbCl or CsCl as contrasted with prolongation by LiCl. The narcotic dosage of ethanol used reduced endogeneous Li+ and increased Cs+ levels in the cerebellum. This massive ethanol dosage exerted little effect on the distribution of exogenously administered Cs+ with exception of the striatum which continued to show a high content of Cs+. This may have contributed to partial antagonism of ethanol-depressant action and to restoring of motor function, i.e., rapid regaining of righting reflex. The results showed that Cs+ possessed longer biological life time in the brain than Rb+ or Li+ which may be of therapeutic value, i.e., in the use of Cs salts in treatment of brain tumors and in conjunction with psychoactive agents provided the respective chemotherapeutic and antidepressant properties of CsCl have been established.

Animals↗
PubMed1984

Modulation of nitrogen dioxide toxicity by lithium.

The effect of short-term intake of LiCl in drinking fluid on NO2 toxicity was studied in mice as a function of mortality and of specific activities of mouse liver alcohol dehydrogenase (L-ADH) and aldehyde dehydrogenases (L-ALDH). Pretreatment with LiCl for 10 days decreased mortality in mice exposed to 60 to 70 PPM NO2 for 6 hr compared to controls. Pretreatment with LiCl for 10 days under continued exposure to 5 PPM NO2 resulted in a decrease in liver weight compared to control. Lithium treated mice exposed to NO2 showed less gain in body weight than the controls treated with LiCl and exposed to air. The latter group showed an induction of mitochondrial but not cytoplasmic L-ALDH and the NO2 exposure did not alter endogenous L-ALDH from corresponding controls. This induction of mitochondrial ALDH was associated with an increase in both Vmax and the apparent Km. Exposure to NO2 for 10 consecutive days resulted in inhibition of cytoplasmic L-ALDH. The data suggest that Li+ antagonized NO2 toxicity. A possible mechanism for reduction of NO2 toxicity by LiCl may be due to Li+ action on stabilizing cell membranes and/or modifying intercellular pulmonary response to NO2 injury.

Acetaldehyde↗
PubMed1984

Cesium: a bibliography update.

A brief outline of both industrial and medicinal uses is given. This is followed by a survey of literature on cesium salts for the period between January 1981 to May 1984. The bibliography searched indicates an interesting pharmacological and behavioral effect for Cs-salts in addition to its well known physiological and itopic effects. A pattern of clinical trials suggests the potential of cesium salts in certain cancer therapies, affective disorders, tumor imaging, radiotherapy and certain cardiovascular usages. The need for continued probing into the biological activity of this alkalimetal is suggested.

Bibliographies as Topic↗
PubMed1984

Effect of separate and combined treatment with chlorpromazine and lithium on mouse liver alcohol and aldehyde dehydrogenase.

The effect of short-term intake of LiCl in drinking water on mouse liver alcohol dehydrogenase (L-ADH) and aldehyde dehydrogenase (L-ALDH) was studied in the albino and in the C57BL mouse strain. The Li-treatment induced initially mitochondrial L-ALDH which was followed by L-ADH in the albino mouse. This was not apparent in the C57 mouse strain. There was an induction of hepatic L-ADH and L-ALDH in the C57BL mouse subsequent to short-term administration of chlorpromazine (CPZ). Coadministration of LiCl with CPZ resulted in moderate enhancement of enzymatic activity per mg wet liver tissue from corresponding controls. Chlorpromazine inhibited rat liver and testicular ADH when tested in vitro. Both cytoplasmic and mitochondrial ALDH were not altered by CPZ in vitro. The results suggest that alcohol consumption during treatment with both drugs studied could evoke metabolic adverse reactions which appear to be both species and strain dependent.

Alcohol Oxidoreductases↗