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Biomedical subjects

B H Ali

Publications and source records attributed to B H Ali.

At least 145 records · Page 8Linked to original sources
PubMed1984

The effect of furazolidone on fertility of male chickens.

In mature chickens, furazolidone (0.4% w/w, 10 days) decreased the weight of the testes, but did not affect significantly the concentrations of testosterone in testes and plasma, nor the concentrations of ascorbic acid, protein or cholesterol in the testes. Feeding furazolidone at a concentration of 0.08% w/w for 10 days decreased significantly the weights of the testes, wattles and combs. Treatment also produced significant reductions in the concentration of testosterone in plasma and testes, and some reductions in ascorbic acid, protein and cholesterol concentrations in the testes. Administration of furazolidone by crop tube at doses of 40 or 80 mg/kg for five days caused significant decreases in the concentrations of testicular and plasma testosterone, and reductions in ascorbic acid, protein and cholesterol concentrations in the testes. The sizes of the testes, wattles and combs were also significantly reduced. Monoamine oxidase activity in the testes was significantly inhibited by furazolidone. In all the treated birds testicular concentrations of 5-hydroxy-tryptamine were significantly raised, except in those fed the drug at a dose of 0.04% w/w for 10 days.

Animals↗
PubMed1984

Acute toxicity of samorin (isometamidium chloride) in rabbits.

Oral administration of samorin (isometamidium chloride) to rabbits in single oral doses of 6.25, 12.5, 25 and 50 mg/kg produced signs of toxicity which were dose-dependent. These were restlessness, hyperaesthesia, tremors, convulsions and finally death. Post mortem examination revealed fatty change, congestion and haemorrhage in many organs. Histopathological examination of liver, brain, kidneys and lungs showed severe circulatory changes and cellular damage. Measurement of serum constituents confirmed the presence of hepatic and renal damage. Samorin produced a marked fall in the erythrocyte count and the haematocrit values of all the treated rabbits, and in doses of 25 and 50 mg/kg it also increased the osmotic fragility of the erythrocytes.

Animals↗
PubMed1984

Plasma and histological changes in furazolidone treated chickens.

Chickens were treated orally with furazolidone at dose rates of 40 or 80 mg kg-1 for five days or fed the drug at concentrations of 0.04 per cent w/w or 0.08 per cent w/w for 10 days. Plasma constituents, liver, heart, kidney, cerebrum, cerebellum and testes were examined. Furazolidone at the recommended therapeutic dose rate of 0.04 per cent w/w for 10 days or at a dose rate of 40 mg kg-1 for five days produced no significant changes in morphology or plasma parameters measured. At a dose rate of 0.08 per cent w/w for 10 days or 80 mg kg-1 for five days, furazolidone produced significant decreases in the concentrations of total protein and cholesterol and tended to increase the activity of cholinesterase. In the plasma, concentrations of potassium increased and concentrations of sodium decreased. Histologically, congestion and some degenerative changes were observed in the tissues examined.

Animals↗
PubMed1984

Preliminary pharmacokinetic study of isometamidium chloride in camels.

Isometamidium chloride was given to camels at a single intravenous dose rate of 0.5 or 1 mg kg-1 and the plasma drug concentration measured spectrophotometrically at frequent intervals for up to 48 hours. Isometamidium chloride concentrations were found to be 9.8 +/- 0.2 and 8.7 +/- 0.2 micrograms ml-1 half an hour after treatment with 1 and 0.5 mg kg-1, respectively, and 1.7 +/- 0.3 and 0.7 +/- 0.3 micrograms ml-1 after 24 hours. No measurable drug concentration was found 48 hours after dosing.

Animals↗
PubMed1984

Toxicity of furazolidone to Nubian goats.

Male Nubian goats were given furazlidone orally at daily doses of 40, 80, 160 and 320 mg/kg for up to 10 days. Animals given 160 and 320 mg/kg became anemic, and showed anorexia, hyperexcitability, uneasiness , backward walking, locomotory disturbances and circling. These animals died within 5 to 7 days of treatment. Postmortem examination showed mild congestion in brain, and fatty change in liver and kidneys. There was histopathological evidence of hepatic and renal damage, and some necrosis in brain and adrenals. Biochemical examination of serum confirmed the presence of hepatic and renal damage. Goats given furazolidone at daily doses of 40 and 80 mg/kg showed similar signs as above, but to a lesser degree. They were killed at the end of the experiment (10 days). The signs of furazolidone intoxication resembled those of cerebrocortical necrosis (thiamine deficiency in ruminants). Therefore, thiamine (100 mg/animal) was injected iv daily to goats receiving 320 mg furazolidone/kg. The vitamin ameliorated the severity of the drug toxicity.

Animals↗
PubMed1983

Some pharmacological and toxicological properties of furazolidone.

The pharmacological and toxicological properties of furazolidone have been briefly reviewed. Among the most important pharmacological actions of furazolidone is the inhibition of mono- and diamine oxidase activities, which seem to depend, at least in some species, on the presence of the gut flora. The drug also seems to interfere with the utilization of thiamin, which is probably instrumental in the production of anorexia and loss of body weight of the treated animals. Furazolidone is known to induce a condition of cardiomyopathy in turkeys, which could be used as a model to study alpha 1-antitrypsin deficiency in man. The drug is most toxic to ruminants. The toxic signs observed were of nervous nature. Experiments are in progress in this laboratory to try to explain the mechanism(s) by which this toxicity is brought about. It is uncertain whether the use of furazolidone at the recommended therapeutic dose would result in drug residues in tissues of treated animals. This is a matter of public health importance as the drug has been shown to possess a carcinogenic activity. It is important that a simple and reliable method of identification and estimation of furazolidone residues be devised. More work is needed to elucidate the mode of action and biochemical effects caused by the drug in both the host and the infective organisms.

Adrenal Glands↗
PubMed1983

The effect of nitrofurazone on the thiamin status of chickens.

Nitrofurazone, given orally at doses of 10 and 20 mg/kg for seven days, decreased the activity of erythrocyte transketolase (TK) and increased the activation of TK by thiamin pyrophosphate (TPP effect %). Nitrofurazone also decreased the feed intake and growth of the chickens, and increased the concentrations of lactate and pyruvate of their blood. It was concluded that nitrofurazone has induced thiamin deficiency in the treated birds. Pair-feeding experiments showed that the decreased growth was due to anorexia, and that the effects produced by nitrofurazone treatment on the thiamin status were attributable to the drug, per se, and not to anorexia. Thiamin (100 micrograms/kg, injected subcutaneously), when given concomitantly with nitrofurazone, was effective in preventing the development of thiamin deficiency.

Animals↗
PubMed1983

The anti-diamine oxidase effect of furazolidone in rabbits.

1. Furazolidone (50 mg/kg for 5 days) given orally to rabbits produced a significant inhibition of diamine oxidase (DAO) activity in various tissues. 2. Suppression of the rabbits' gut flora by oxytetracycline treatment significantly reduced the DAO inhibitory effect of furazolidone, suggesting that the gut flora may be involved in the transformation of furazolidone into an active DAO inhibitor.

Amine Oxidase (Copper-Containing)↗
PubMed1983

The effect of furazolidone on the adrenal glands of the chicken.

In the chicken, the weights of the adrenal and thyroid glands (as percentages of body weight) were selectively increased following administration of furazolidone (0.04 per cent w/w in the feed, 10 days). The increase in the weight of the adrenal glands most probably represents hypertrophy of the cortex, as the amount of catecholamines in the glands was unaffected by furazolidone. Furazolidone (0.04 per cent w/w, 10 days) produced a small reduction in the concentration of cholesterol in the adrenals. The concentration of ascorbic acid in the gland was unaffected by the drug.

Adrenal Glands↗
PubMed1982

Anorexia and antagonism of thiamin utilization in poultry treated with furazolidone.

Furazolidone (0.4% w/w in the feed, 10 days) reduced the feed intake and growth in 9 week old chickens, and increased the amount of 5-hydroxytryptamine (5-HT) in the brain. The drug also increased the stimulation of transketolase activity by thiamine pyrophosphate (TPP) in lysed blood cells (TPP effect), and the concentrations of pyruvate and lactate in the blood. Experiments with pair-fed birds showed that the reduction in feed intake in furazolidone-treated chickens could account for the reduced growth. The drug also produced anorexia in ducklings and turkey poults. In chickens, the anorectic action of furazolidone was unaffected by methergoline (1 mg/kg, twice daily, I.M), and in ducklings furazolidone did not consistently produce anorexia, although it always inhibited monoamine oxidase (MAO) activity in the brain. These observations suggest that the anorectic action of the drug was not tryptaminergic in nature. The increase in the TPP effect found in preparations from furazolidone-treated chickens was absent in preparations from pair-fed birds on unmedicated feed. Thus the TPP effect could be used as an indicator of the effect of the drug on the thiamine status of chickens. However, the increase in the concentrations of pyruvate and lactate in blood was found both in furazolidone-treated birds and pair-fed birds on unmedicated feed, showing that they were attributable to the reduction in feed intake. The TPP effect in furazolidone-treated chickens, 14-49 +/- 2.33% (n = 10), was sufficient to suggest a mild deficiency of thiamin pyrophosphate. Thiamin, given at a dosage above the requirement of the vitamin for chickens, did not reduce the anorexia or the TPP effect of furazolidone-treated birds, although it stimulated the feed intake and growth of birds on unmedicated feed. It is proposed that furazolidone antagonized the utilization of thiamin, perhaps by inhibiting its phosphorylation. Following the withdrawal of furazolidone, the TPP effect returned to the control value and the rate of growth of the birds increased and matched that the controls. Thus the effect of the drug was reversible. Addition of furazolidone to the feed at a concentration of 0.01% w/w for 28 days did not produce anorexia in chickens or affect the amount of 5-HT in the brain. Thus at this level, it is unlikely that the drug would produce adverse effects in poultry.

Animals↗
PubMed1980

Inhibition of monoamine oxidase by furazolidone in the chicken and the influence of the alimentary flora thereon.

1 The addition of furazolidone to the feed at the therapeutic level (0.04% w/w, 10 days) inhibited monoamine oxidase (MAO) activity by 47 to 72% in chicken duodenal mucosa, heart and brain, but in the liver the enzyme activity was unaffected by the treatment. 2 Furazolidone (200 mg/kg) administered by crop tube inhibited MAO activities in duodenal mucosa, liver, heart and brain. 3 Furazolidone (200 mg/kg) injected intramuscularly did not inhibit MAO activity in the chicken. 4 Pretreatment of the chickens with intramuscular neomycin did not antagonize the inhibition of MAO activity produced by furazolidone (200 mg/kg, crop tube). 5 Pretreatment with neomycin by crop tube to suppress the alimentary flora significantly reduced the effect of furazolidone on MAO activity, suggesting that the drug was transformed by the alimentary flora to an active metabolite which subsequently inhibited MAO activity in other organs. 6 Furazolidone in the feed (0.04% w/w, 10 days) or administered by crop tube (200 mg/kg) had no effect on the activity of aminopyrine demethylase in chicken liver. 7 The activity of aspartate transaminase in plasma was unaffected by the addition of furazolidone to the feed (0.04% w/w, 10 days).

Aminopyrine N-Demethylase↗
PubMedDate not supplied

Toxicological studies on the leaves of Avicennia marina (mangrove) in rats.

Haematological, biochemical and pathological effects in rats produced by the salt-tolerant plant Avicennia marina given at oral doses of 1 or 4 g kg(-1) for three consecutive days or 0.5 g kg(-1) day(-1) for 28 consecutive days are reported. No overt behavioral changes, moribundity or mortality were seen in either of the two experiments. A dose of 1 g kg(-1) did not affect significantly either body or liver weights. However, at a dose of 4 g kg(-1) the extract reduced both body and liver weights. The extract at both doses significantly increased leucocyte (mainly neutrophil) counts but did not affect significantly erythrocyte counts, haemoglobin concentration or the haematocrit. Except for a slight, but statistically significant, decrease in plasma glucose concentration and an increase in Na, Ca, Cu, Mg and cholesterol concentrations and aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, the extract exerted no significant effects on plasma biochemistry. The treatment produced dose-related mild cellular degeneration in the liver and congestion in the central veins. There were also prominent Kupffer's cells and monocellular infiltrations. In the kidneys there was shrinkage and cellular degeneration of glomeruli and patches of medullary haemorrhage. In the spleen a slight activation of the germinal centre in the white pulp was noted. Subchronic treatment with the extract did not affect significantly the body and liver weights, the water intake, faecal and urinary output, leucocyte and erythrocyte counts, haemoglobin or haematocrit. There was a significant decrease in the number of platelets and an increase in the number of neutrophils. No significant changes in plasma biochemistry were observed, except for a 15% increase in AST activity. Subchronic treatment produced a significant reduction in glutathione concentration, amounting to about 20%. Histopathological findings after the subchronic treatment were similar in nature but milder than those seen after the acute treatment.

Administration, Oral↗