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Biomedical subjects

S H Gilani

Publications and source records attributed to S H Gilani.

At least 19 recordsLinked to original sources
PubMed1990

Teratogenicity of metals to chick embryos.

The present study examines the effects of heavy metals on chick embryogenesis. The metals included were cadmium, arsenic, cobalt, copper, indium, iron, manganese, and molybdenum. Salts of each of the metals were dissolved in saline and injected into the air sacs on d 2 of incubation. Dose levels varied with the metal to be tested. Control eggs were injected with an equivalent volume of saline (0.1 ml/egg). On d 14, the live embryos were removed from the eggs and examined for gross malformations. From the LD50 values, the toxicity relationship between the metals is cadmium greater than arsenic greater than cobalt greater than copper greater than indium greater than molybdenum greater than manganese greater than iron. The LD50 values were 3, 9, 38, 58, 121, 333, 765, and 1185 micrograms/egg, respectively. The gross malformations observed were reduced body size, micromelia, twisted neck, hemorrhage, everted viscera, and microphthalmia. Arsenic and cobalt were observed to be more teratogenic than other metals. This study showed that the metals tested were both toxic and teratogenic to varying degrees in chick embryogenesis.

Animals↗
PubMed1989

The effects of minoxidil on the development of the chick embryo.

The effects of minoxidil were studied on chick embryos of 24 and 48 hours of incubation. Minoxidil (3%) was injected into the air sacs of the eggs at doses of 20, 30, 40, and 50 microliters per egg. The controls received 100 microliters of physiological saline. All the embryos, including controls, were examined at day 13. The total number of eggs used in this study was 300. At 24 hours incubation, the percentage of survival ranged from 87 to 21 as the dosages of minoxidil were increased from 20 microliters to 50 microliters per egg (controls = 87%). The survival of the embryos ranged from 79% to 9% after the 48-hour treatment with the similar dosages of minoxidil utilized for the 24-hour group (controls = 83%). A low incidence of gross malformations such as twisted limbs, abnormal beak, short neck and everted viscera were observed; however, the increased incidence was not statistically significant when compared to controls. Body hemorrhage and edema were of high occurrence among the treated embryos. These effects are probably secondary to the known pharmacological effects of minoxidil. The frequency and types of gross malformations did not vary much in the 24 or 48-hour treated groups.

Animals↗
PubMed1987

Embryopathic effects of ethanol in the chick.

The chick embryo is considered a highly sensitive system for the screening of drugs for possible teratogenicity. The effects of varying concentrations of ethanol on the early development of chick embryos were studied. The mean weight of embryos exposed to ethanol was reduced compared to that of the control groups, but the difference was not significant. However, embryolethality and the incidence of abnormal embryos were significantly increased and related to the dose of ethanol.

Abnormalities, Drug-Induced↗
PubMed1986

Acrolein and embryogenesis: an experimental study.

The effects of acrolein were studied on the chick embryos of 48 and 72 hr of incubation. Acrolein was dissolved in physiological saline and injected into the air sacs of the eggs at doses ranging from 0.001 to 0.1 mg per egg. The controls received and equal amount of saline only (0.1 ml per egg). All the embryos including controls were examined at Day 13. In all, 600 eggs were utilized for this investigation. At 48 hr incubation, the percentage survival ranged from 80 to 0 as the dosage of acrolein was increased. Embryonic mortality following 72 hr incubation did not increase significantly at any dose level. Gross malformations such as short and twisted limbs, everted viscera, microphthalmia, short and twisted neck, and hemorrhage over the body were observed. The frequency and the types of gross abnormalities did not vary much in the 48- or 72-hr-treated groups. The incidence of malformation in the controls was low. The results of this study indicate that acrolein is embryotoxic at higher doses and moderately teratogenic to chick embryogenesis.

Abnormalities, Drug-Induced↗
PubMed1986

Chick embryonic development following exposure to caffeine and nicotine.

Because cigarette smoking is considered to be deleterious to the fetus and caffeine is held in suspect as a potential human teratogen, the combined effects of caffeine and nicotine on early chick embryos were investigated. Treatment of the embryos at 48 h incubation with both caffeine (1 mg) and nicotine (1 mg) resulted in a high incidence of embryonic death and developmental defects. At 72 h incubation teratogenicity was potentiated following the same treatment. Embryonic growth was not affected. Embryotoxic interactions of this nature might account for congenital anomalies of doubtful etiology.

Abnormalities, Drug-Induced↗
PubMed1986

Chick embryonic development following exposure to ethanol and pyrazole.

The mechanism of alcohol-induced dysmorphogenesis is not clear. Pyrazole is a potent inhibitor of alcohol dehydrogenase. Treatment of chick embryos at 96 h incubation with pyrazole (0.1 mg) and ethanol (0.1 ml, 40-60% v/v) enhanced the embryopathic response, compared with individual treatments. The results suggest that ethanol itself is embryotoxic.

Animals↗
PubMed1985

Embryotoxic effects of doxorubicin and N-trifluoroacetyladriamycin-14-valerate (AD-32).

Anthracyclines are mutagenic, carcinogenic, and also cardiotoxic. Concern has been shown over the use of anthracycline anticancer drugs during pregnancy as these may be teratogenic to the human fetus. We have performed a series of experiments using the chick embryo to investigate and compare the toxic and teratogenic effects of doxorubicin (DX) and its new analog N-trifluoroacetyladriamycin-14-valerate (AD-32). DX and AD-32, dissolved in 1:1 emulphor/ethanol and diluted to 1:4 with water, were injected into the air sac of white leghorn chick eggs at dose levels of 1-20 micrograms (DX) and 5-100 micrograms (AD-32) per egg. Eggs received a single injection of the drugs on days 1 and 2 of incubation. Control eggs were injected with an equivalent volume of the drug vehicle (0.05 ml per egg). Both of the drugs caused embryonic death, stunted growth, and various gross morphological malformations. Surviving embryos were sacrificed when they reached 13 days of incubation. The LD50 values for days 1 and 2 were as follows: (DX, 2.5 micrograms/egg on day 1 and 0.9 microgram/egg on day 2; AD-32, 10.6 micrograms/egg on day 1 and 11.8 micrograms/egg on day 2). Stunting of growth, a common anomaly with both drugs, decreased sharply from day 1 to day 2. The studies demonstrate that both DX and AD-32 are toxic and teratogenic during the period of early organogenesis in the chick embryos. However, the toxic and teratogenic potentials of DX and AD-32 differ quantitatively. AD-32 is a more potent teratogen than DX when injected on day 1.

Abnormalities, Drug-Induced↗
PubMed1985

Embryopathic effects of ethanol and caffeine in the chick.

The combined effects of ethanol (20 and 40%, 0.1 ml/egg) and caffeine (0.5 and 1 mg/egg) on early chick embryos were investigated. After treatment with 0.5 mg caffeine and 20% ethanol at 48 h incubation, teratogenicity was potentiated, but without affecting embryonic growth. Embryotoxic interactions of this nature might account for congenital defects of doubtful etiology.

Abnormalities, Drug-Induced↗
PubMed1978

Cardiac myopathies in neonatal lambs: histological and histochemical studies.

White muscle disease (WMD), a selenium-responsive cardiac myopathy in neonatal lambs has been described from southern Iran. 15 lambs in terminal condition were referred to our lab. All the lambs were observed with the affected hearts. The lambs examined were between the postnatal ages of 1 week and 3 months. Gross changes included chalky-white appearance of entire endocardium of right ventricle and subendocardial plaques in the interventricular septum and left ventricular wall. Histologically the affected myofibrils showed swelling, acidophilia, fragmentation, segmental and patchy myonecrosis, round muscle cell nuclei, loss of sarcoplasm and sarcolemmal collapse. Purkinje fibers were relatively unaffected. Histochemical studies including Von Kossa and other stains indicated marked deposition of calcium salts in the cytoplasm of the damaged myofibrils. Calcium salts appeared as uniform, fine granules in relation to individual fiber striations. It appears that rapid accumulation of calcium into the damaged cells possibly interferes with the mitochondrial activity. As mitochondria bind excessive calcium, their capacity to respire and phosphorylate is depressed thus causing myocardial necrosis. The cardiac myopathy noted in our investigation is probably due to selenium deficiency in the soil of southern Iran. When selenium was given, it resulted in the fast recovery of the affected neonatal lambs. Moreover, no further cases of this disease (WMD) were reported after such treatments.

Animals↗
PubMed1977

Disposition of 14C-nicotine in the fertilized chick egg.

14C-Nicotine-HCl (4.5 mg) was injected into the air space of chick eggs after one day of incubation and the distribution of radioactivity measured on days 3, 5, 7 and 12. By day 3, 98% of the dose had passed from the air space into the egg, proper. The quantity of nicotine in the yolk was highest on day 3 (74% of dose) and decreased steadily until day 12 (52%). The quantity in the albumen increased from 16% on day 3 to a maximum on day 7 and remained constant at 34% until day 12. The embryo contained 0.03% of the nicotine on day 3, and this level increased to 5% by day 12. Nicotine in the allantois increased throughout the study period (0.01% on day 3 to 3% on day 12). Although only 5% of the dose was present in the embryo, the highest concentrations within these components of the embryo ranged from a minimum of 0.85 microng nicotine/mg dry wt in the heart to a maximum of 2.00 microng nicotine/mg dry wt in the carcass. These levels within the embryo were two to five times higher than the greatest concentrations in the yolk and albumen. The dynamics of nicotine passage from the air space into other components of the fertilized chick egg were clarified. Whereas the conventional expression of teratogenic doses of drugs in chick eggs (i.e., ppm of egg weight) assumes that the compound is distributed uniformly, this study indicates that such expressions are inaccurate.

Animals↗
PubMed1977

The effect of propranolol upon chick embryo cardiogenesis.

The teratogenic effects of propranolol HCl on cardiac development were studied in chick embryos of days 3 and 4 of incubation. Propranolol was injected into the yolk sac at doses ranging from 0.05 to 0.6 mg per egg. All the treated and control embryos were examined on day 7. The LD50 for the embryos treated on the 3rd and 4th day was 0.15 and 0.35 mg per embryo, respectively. Cardiac anomalies such as aortic stenosis ventricular septal defects and common truncus arteriosus were observed. Other malformations included atrial septal defects, thin atrial wall and defects of the pulmonic, aortic and atrioventricular valves. The incidence of cardiac anomalies in the controls was very low. Propranolol was observed to slow the heart rate in the experimental embryos. It is suggested that slowing of heart rate at the early stages of heart development caused aberrant bloodstream flow patterns which probably resulted in the genesis of cardiac anomalies. The results of this study indicate that propranolol has teratogenic effects on chick embryo cardiogenesis.

Abnormalities, Drug-Induced↗
PubMed1975

Nicotine effects on the acid mucopolysaccharide content of chick embryo cardiac jelly.

Histochemical studies were made on the developing chick embryo heart to determine the effects of nicotine on acid mucopolysaccharide content during the critical stages of the cardiac morphogenesis. Two-day old embryos were injected with the dosages of nicotine ranging from 1.5 to 3 mg per embryo. The embryos were studied on the 3rd and 4th days of incubation. For an evaluation of acid mucopolysaccharides, the staining procedures of Mowry (1958) and Saunders (1964) were employed. It was found that nicotine decreases the content of acid mucopolysaccharide in the developing cardiac jelly. In the control embryos, the cardiac tissues picked up very intense coloration. At lower dosages (Group A; 1.5 mg/egg), the staining response of the treated heart tissues containing acid mucopolysaccharides was moderate as compared to the control embryos. At higher dosages (Group B; 3 mg/egg), the cardiac tissues were faintly colored as compared to the embryos of Group A. It is possible that the cardiac lesions previously reported in the chick embryos following the administration of nicotine (Gilani, 1971) are due to the reduction of the amount of acid mucopolysaccharides in the developing cardiac jelly--a susceptible period of the genesis of heart.

Animals↗
PubMed1975

Fine structural changes in embryonic chick heart ventricle induced by lead poisoning.

The embryonic chick heart ventricle of day 11 was studied electron microscopically to learn the structural changes that develop in lead poisoning. The chick embryos were administered with 0.015 mg/egg of lead acetate at day 2. The most pronounced changes observed in the ventricle were: malformed mitochondria, disorganized, short and scanty myofibrils and abundance of swollen vacuoles. The ultrastructure of the ventricle from the control chick embryos was normal. The most frequent change noted in the ventricular tissue was an alteration in the myofibrils. This study indicates that electron microscopic changes can be induced in the embryonic chick heart ventricle by lead poisoning.

Animals↗