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Biomedical subjects

F S Messiha

Publications and source records attributed to F S Messiha.

At least 73 records · Page 4Linked to original sources
PubMed1984

Hepatic and testicular aldehyde dehydrogenase in tumor-bearing mice.

The interrelationship between certain dehydrogenases and a hepatic tumor was studied in mice. A rapidly growing hepatoma, Novikoff hepatoma, was transplantable from rats to mice after serial passages in Sprague-Dawley albino mice. Mice inoculated with viable tumor cell suspension were sacrificed 14, 18, 21 or 34 days thereafter. Hepatic cytoplasmic and mitochondrial aldehyde dehydrogenase (ALDH) were measured in addition to liver alcohol dehydrogenase (ADH) and testicular ALDH. Hepatic cytoplasmic and mitochondrial ALDH were markedly inhibited from controls at all time periods studied. Likewise, testicular ALDH was inhibited from respective controls in Novikoff hepatoma-bearing mice. No changes were measurable in hepatic ADH of hepatoma-bearing mice. The enzyme kinetics studied show a reduction in Vmax and an alteration in the apparent Km 34 days after tumor inoculation. Further analyses of hepatic mitochondrial ALDH showed that the inhibition was similarly present in the enzyme with the low and the high Km property. The results suggest that changes in the specific activity and property of ALDH may be a useful tool as a biochemical concomitant to both development and progression of the hepatoma studied.

Alcohol Oxidoreductases↗
PubMed1984

Effect of nutmeg on ethanol and d-amphetamine-produced alteration of locomotor activity in the mouse.

A behavioral performance test was used to assess the effect of a mild nutmeg extract on spontaneous locomotor activity of the mouse. The nutmeg extract was administered intraperitoneally once daily for 17 consecutive days and only moderately reduced motor activity from corresponding control. A nutmeg dosage devoid of action on motility was chosen for short-term administration to mice. These nutmeg treated mice and the saline controls received either a single depressant dosage of ethanol or a stimulant dose of d-amphetamine. Nutmeg treated mice showed potentiation of ethanol-mediated depression on motility compared to controls. The d-amphetamine-produced stimulation of locomotor activity was decreased from controls by the nutmeg treatment. The results indicate that the nutmeg extract preparation used contained ingredients which synergistically interacted with alcohol as contrasted with their antagonism to d-amphetamine. The results suggest a CNS depressant action of nutmeg. Such CNS impairment by nutmeg may conceivably contribute to its toxic interaction with certain substances of abuse and may explain, in part, its addictive potential.

Animals↗
PubMed1983

Behavioral and clinical profiles of Tourette's disease: a comprehensive overview.

A brief review of Gilles de la Tourette's disease is presented. The initial part gives an overview of major signs, symptoms displayed, and diagnosis in addition to certain minor concomitant features. The latter conditions included appetite, adaptive function, learning disorders, sexual behavior, sleep disturbances, speech pathology, and tic-related injury. Neurological manifestations, infectious etiology, and genetics were discussed. Treatment modalities are outlined and description of various drug therapy is given in conjunction with rationale of pharmacotherapy and possible underlying mechanism of action. Drug-induced Tourette's-like syndrome was also summarized.

Acetylcholine↗
PubMed1983

Endocrine aspects of lithium therapy in Tourette's syndrome.

The use of Lithium Carbonate (Li2CO3) therapy in Gilles de la Tourette syndrome is reported in one patient. The patient, a 22-year-old male, was treated with a daily dose of 900 mg of Li2CO3 to attain therapeutic blood serum lithium concentration between 0.76 and 0.87 mEq/L. Renal function tests, urine analysis and thyroid function tests were monitored in addition to determinations of serum gonadotropins and testosterone concentrations throughout the 8 months of the study. The neuroendocrine measurements indicate blunting of Thyrotropin Stimulating Hormone (TSH) response, to Thyrotropin Releasing Hormone (TRH) stimulation test, which may be due to lithium therapy. The patient's growth and development were normal. This case represents the first report of blunting of TSH response to TRH in Tourette's disease. The fact that this disease has an onset during childhood suggests the importance of monitoring various endocrine functions during lithium therapy.

Adult↗
PubMed1983

Clinical uses of lithium salts.

A comprehensive overview of the clinical aspects of lithium therapy is presented. Emphasis is placed on recent developments regarding the clinical uses of Li2CO3 in non-psychiatric conditions. The established efficacy of the drug in the treatment and prophylaxis of mania and bipolar affective disorders is noted, and the evidence supporting the use of lithium salts as a prophylactic agent in unipolar depression, aggressive behavior, schizophrenic disorders and organic brain dysfunction is discussed. The use of lithium carbonate in various disorders of movement and in certain extrapyramidal diseases is summarized, as are the results of its trials in alcoholism and drug abuse. In addition, uses of Li2CO3 in asthma, thyroid diseases, granulocytopenia, headache, bowel disease, anesthesiology, cardiology, and sleep disorders are summarized. The data suggests the potential effectiveness of Li2CO3 in a variety of clinical conditions other than those for which it is classically indicated, provided more detailed double-blind studies are performed.

Affective Disorders, Psychotic↗
PubMed1983

Extrapyramidal disorders: a possible underlying mechanism.

In vivo and in vitro studies have been presented to suggest an interrelationship between drugs used in the management of, or known for their induction of extrapyramidal disorder and certain dehydrogenase enzymes involved in this metabolic pathway of the biogenic amines. This relationship is discussed to advance a tentative hypothesis explaining a possible underlying mechanism and to provide an explanation for the implication of alcohol consumption in worsening of extrapyramidal symptoms during certain pharmacotherapy. The major neutral metabolites of the biogenic amines acted as substrate to or induced rat liver alcohol dehydrogenase (L-ADH) and drugs used in the management of tardive dyskinesia similarly induced L-ADH. This induction of L-ADH could enhance the metabolic biotransformation of the neutral metabolites of the monoamines. Conversely, drugs known to evoke extrapyramidal dyskinesias inhibited rat liver aldehyde dehydrogenase (L-ALDH). This inhibition of ALDH may give rise to toxic condensation products between biogenic amine aldehydes and their precursors which may be implicated in certain dyskinesias. It is proposed that one of the mechanisms underlying the biogenic amine involvement in the pathogenesis of certain extrapyramidal diseases may include a critical balance between their reductive and oxidative routes of metabolism.

Alcohol Dehydrogenase↗
PubMed1983

Effect of alkali metals on chlorpromazine toxicity in the mouse.

The effect of short-term injection of chlorpromazine alone or combined with either LiCl or CsCl (1 mEq/kg/day) in organ toxicity was studied in the albino male mouse. Chlorpromazine was administered by gradual dose build-up regimens from 5 mg/kg to 50 mg/kg which was attained over a 40-day period followed by abrupt drug withdrawal for a subsequent 25-day observation period. Histological evaluation of 10 tissues selected indicates that the liver was the target organ. The Li-treatment resulted in variable liver lobular size with loss of cell definition and the kidney showed focal lymphatic aggregates related to vascular channel. Chlorpromazine-treated mice displayed variation in liver nuclei size and in cell structure definition. Combined injection of LiCl with the phenothiazine drug resulted in alteration in size of liver nuclei with a slight midlobular distribution. Minimal changes in lobular liver cells were noted subsequent to the Cs-treatment. This is compared to some dilation of liver central veins and few variations in hepatocyte size after combined injection of CsCl with chlorpromazine. There was a reduction in body weight of animals treated with the LiCl and chlorpromazine combination compared to that of mice receiving the chlorpromazine alone or in combination with CsCl. A rebound in body weight loss occurred during drug withdrawal in mice pretreated with chlorpromazine alone or combined with CsCl but not in mice coadministered LiCl with chlorpromazine. Mortality score indicates a profound lethal effect during administration of LiCl with the high dosage of the chlorpromazine used which was persistent during drug withdrawal.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Chlorpromazine and lithium interaction: a biochemical and histological study.

Biochemical and histological studies on the effect of separate and combined administration of LiCl and of chlorpromazine (CPZ) on female C57BL/6J mice were performed. Mice were divided into 4 groups. One group was given an intraperitoneal injection daily of CPZ HCl, 5 mg/kg for 4 days followed by 4 more days of a daily dosage of 10 mg/kg. A second group was maintained on 0.4% (w/v) LiCl solution as the sole drinking fluid for 8 consecutive days and a third group received the same LiCl solution but with daily CPZ injection as the initial group for 8 days. The fourth group served as saline-controls. Hepatic liver alcohol dehydrogenase was induced by combined drug treatment from respective controls. The Li-treatment inhibited mitochondrial liver aldehyde dehydrogenase, and coadministration of CPZ with LiCl antagonized this effect. Mice treated with CPZ showed corneal cellularity and mitotic figure appearance without inflammation. The LiCl treated mice displayed variations in base corneal cell size, shape and pigmentation with aggregation of the nuclei, and the presence of mitotic activity inflammation. Mice receiving combined drug treatment showed similar corneal alterations, but mitotic figures were found above base cell layer suggesting an enhanced corneal toxicity. The results suggest a drug-drug interaction phenomenon which may explain some of their adverse reaction when given concurrently.

Alcohol Oxidoreductases↗
PubMed1983

Modification of mouse liver alcohol and aldehyde-dehydrogenase by chlorpromazine.

The in vivo and in vitro effect of chlorpromazine (CPZ) on female mouse liver alcohol dehydrogenase (L-ADH) and mitochondrial aldehyde dehydrogenase (L-ALDH) was studied as a function of illumination conditions. Chlorpromazine was injected once daily in a gradual dose build-up from 5 to 30 mg/kg, i.p., over 21 consecutive days. This resulted in a noncompetitive inhibition of endogenous L-ALDH of mice housed under UV light exposure but not those maintained under standard laboratory fluorescent lighting and receiving identical CPZ treatment. No changes occurred in L-ADH in vivo but a noncompetitive inhibition of mouse L-ADH was determined in the presence of 50 muMol of CPZ in vitro. The results are discussed in reference to possible toxic mechanism underlying CPZ and ethanol interaction.

Alcohol Dehydrogenase↗
PubMed1983

Altered atrial responses to drugs after acute exposure to nitrogen dioxide and/or ethanol.

The responses of atria isolated from four groups of rats: (a) control (air/H2O) and test animals treated with (b) 5 PPM nitrogen dioxide NO2 for 72 hours, (NO2/H2O), (c) 10% ethanol (ET) in water for 13 days, (air/ET), or (d) combination of NO2 and ET (NO2/ET). Isolated atria were tested with norepinephrine and dose response curves determined. The chronotropic responses among groups were not different. However, there were significant differences when tested with pilocarpine and to lesser extent to increased calcium concentration in the bathing medium. Ethanol and/or NO2 attenuates parasympathetic activity possibly by altering receptor numbers or activity. The changes in calcium activity may result from altered calcium channel activity. This data indicates that acute exposure to NO2, ET and/or the interaction between these agents can alter cardiac activity.

Animals↗
PubMed1983

Behavioral, metabolic and histological aspects of lithium and ethanol interaction.

Behavioral, biochemical and histological techniques were used to evaluate the possible interaction between a lithium salt and ethanol. Injection of a single dosage of ethanol into mice pretreated with LiCl for 14 days enhanced spontaneous locomotor activity for the initial 60 min of testing compared to respective control. Drinking of 0.4% of LiCl solution for 25 consecutive days induced hepatic alcohol dehydrogenase (L-ADH) and aldehyde dehydrogenase (L-ALDH). The LiCl treatment increased Vmax of both enzymes in the same order and magnitude. The apparent Km of L-ADH was increased by LiCl while that of L-ALDH remained unchanged from respective controls. Organ histopathology indicates decreased germinal activity of the mouse spleen by the LiCl treatment. A mild chronic perivascular inflammation and slight hypercellularity of the myocardium was also noted in the heart of LiCl-treated mice.

Alcohol Dehydrogenase↗
PubMed1982

Ethanol and simulated high altitude. A study of three mouse strains.

The effect of short-term exposure of three mouse-strains to simulated high altitude (SHA) of approximately 6,000 m was studied. Subjecting C57BL/6J, DBA/2J or albino mouse strains to SHA for 39 days, occurring on alternating days, increased liver weight in the albino mouse compared to controls. The C57BL strain showed increased growth during SHA compared to other mouse strains. Morbidity score was greater in the albino mouse than in DBA mouse with no death occurring in C57BL mice exposed to SHA. Hepatic alcohol dehydrogenase was induced and mitochondrial aldehyde dehydrogenase was inhibited from corresponding controls subsequent SHA exposure by the C57BL and by the DBA mouse strain, respectively. The onset of ethanol-mediated narcosis was decreased from controls subsequent 21 days of SHA exposure by the DBA and by the albino mouse strain. The central depressant action of ethanol, as measured by the duration of ethanol-narcosis, was decreased in the C57BL mice exposed to SHA for 8, 21, or 35 days compared to controls. No apparent changes occurred in duration of ethanol-narcosis in the other mouse strains. The results suggest strain-difference in response to hypobaric conditions.

Acetaldehyde↗