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Biomedical subjects

S F Ali

Publications and source records attributed to S F Ali.

At least 181 records · Page 10Linked to original sources
PubMed1985

Effects of chlordecone administration on brain and pituitary peptide systems.

It has been clearly demonstrated that chlordecone exerts estrogen-like effects on the reproductive system. However, the extent to which the estrogenic activity of this neurotoxicant may contribute to its central nervous system effects is not clear. The purpose of this study was to compare the estrogenic activity of chlordecone and estrogen on the rat hypothalamo-pituitary axis (HPA) by using the pituitary enkephalin system as a model. It was found that the enkephalin system of the anterior pituitary is regulated by circulating estrogen. Ovariectomy caused an increase in the pituitary content of enkephalin and this increase was prevented by estrogen treatment. Administration of estrogen reduced the pituitary content of this peptide in intact male rats. Similarly, chlordecone treatment reduced the pituitary content of enkephalin in a manner identical to that of estrogen. A single injection of chlordecone (75 mg/kg; i.p.) caused a delayed decrease in the enkephalin level of the anterior lobe (but not the posterior lobe) of the pituitary. This effect of chlordecone was selective to male rats since the pituitary enkephalin level of females was not altered by such treatment. Levels of other pituitary hormones such as beta-endorphin, vasopressin, etc., were not decreased. Further studies revealed that the similarities between chlordecone and estrogen could be extended to other pituitary hormones. For example, implantation of estrogen or of chlordecone in ovariectomized rats caused similar changes in serum prolactin and luteinizing hormone levels. Thus, this study demonstrates a clear estrogen-like action of chlordecone on the HPA. Moreover, due to the similarity of both estrogen and chlordecone to anti-dopaminergic agents in altering [Met5]-enkephalin levels in both the pituitary and caudate nucleus it is speculated that a dopaminergic mechanism is responsible for their actions on the enkephalin system.

Aging↗
PubMed1984

Estrogen-like activity of chlordecone (kepone) on the hypothalamo-pituitary axis: effects on the pituitary enkephalin system.

Similarities between the activity of chlordecone and estrogen on the hypothalamo-pituitary axis (HPA) were examined by using the pituitary enkephalin system as a model. A single injection (25 to 75 mg/kg, ip) or repeated injections (2.5 to 10 mg/kg/day for 10 days, ip) of chlordecone caused a time- and dose-related decrease in pituitary [Met5]-enkephalin-like immunoreactivity (ME-LI) in adult rats. Similar to the reported effects of estrogen, chlordecone treatment decreased the levels of ME-LI in the anterior lobe but not in the neurointermediate lobe of male pituitaries. Furthermore, chlordecone failed to alter the pituitary levels of ME-LI in female rats. The level of another pituitary peptide hormone, beta-endorphin, was increased in male rats after chlordecone treatment, indicating some degree of selectivity of this effect. Similarities between chlordecone and estrogen were found with other pituitary hormones, i.e., implantation of diethylstilbestrol or of chlordecone in ovariectomized rats caused qualitatively similar changes in serum prolactin and luteinizing hormone levels. These results suggest that chlordecone qualitatively resembles estrogen in its effect on some HPA peptide systems.

Animals↗
PubMed1984

Effect of gossypol on liver metabolic enzymes in male rats.

The effects of gossypol on liver metabolism were examined in male rats. Gossypol acetic acid was administered to Sprague-Dawley rats intraperitoneally (i.p.) at 5 mg/kg daily, 5 days/week for 2 weeks. The rats were killed 24 h after the last injection. The liver/body weight ratio (-42%), concentration of liver glutathione (-34%), activities of liver alpha-naphthtylacetate esterase (-30%) and DNase (-39%) were significantly decreased when compared to controls. Hepatic beta-glucuronidase (+37%), RNase (+35%) and serum alkaline RNase (+23%) activities were significantly increased. No changes were found in serum transaminases (SGPT, SGOT) or in hepatic RNA and DNA concentration. Elevation of liver and serum RNase activities suggest that gossypol treatment produces some catabolic effects. The depletion of hepatic glutathione and the elevation of beta-glucuronidase activity indicate that gossypol is hepatotoxic when given at this dose for 2 weeks.

Alanine Transaminase↗
PubMed1983

Alterations in retinal neurotransmitter receptors and neuropeptides of the chick by kainic acid and acrylamide.

The effects of intraocular injection of kainic acid and acrylamide upon retinal neuropeptides and high affinity binding sites have been determined in the chick. Kainic acid causes a sharp reduction in Met-enkephalin and somatostatin while neurotensin levels are unchanged. This treatment also lowers the extent of cholinergic muscarinic but not of [3H]naloxone or [3H]spiroperidol binding. In contrast, acrylamide treatment causes major increases of retinal Met-enkephalin and neurotensin concentrations. The binding of [3H]naloxone is also increased, and no reductions of any peptide or binding intensity were observed. The results indicate the plasticity of retinal neuropeptide levels and the selectivity with which these can be modulated.

Acrylamide↗
PubMed1983

Effect of acrylamide on neurotransmitter metabolism and neuropeptide levels in several brain regions and upon circulating hormones.

The effect of acute and subchronic acrylamide treatment on levels of dopamine, serotonin, and their metabolites was determined in several brain regions of the rat. Concentrations of several neuropeptides and circulating hormones were also measured. Both a single and repeated doses of acrylamide resulted in elevated levels of 5-hydroxyindolacetic acid in all regions studied (frontal cortex, striatum, hippocampus, brain stem, and hypothalamus). Changes in regional content of other monoamines were much less pronounced. Turnover studies following pargyline blockage of monoamine oxidase, suggested results were due to increased rates of serotonin turnover in acrylamide-treated rats. Changes in neuropeptide levels were only detected in the hypothalamus where a single acrylamide treatment caused elevated levels of beta-endorphin and substance P, and in frontal cortex where met-enkephalin levels were higher after repeated acrylamide injection. Such repeated injection caused a major depression in plasma levels of testosterone and prolactin.

Acrylamide↗
PubMed1983

Correlation of neurochemical and behavioral effects of triethyl lead chloride in rats.

Adult male Fischer-344 rats were dosed sc with 1 or 2.5 mg/kg of triethyl lead chloride (TEL) for 5 consecutive days. One week after the last dose, TEL-exposed rats had decreased Met-enkephalin in the hypothalamus, septum, and frontal cortex, while substance P was decreased in the hippocampus and frontal cortex. Dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) in the caudate nucleus were not altered by TEL nor were serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) in the caudate nucleus, hypothalamus, hippocampus, or frontal cortex. In a second experiment, rats were dosed with 1.75 mg/kg sc for 5 days. Subsequent assay of brain tissue indicated that TEL decreased met-enkephalin levels in the septum of rats one and seven days after cessation of dosing; effects on substance P were not observed. TEL-induced decreases in Met-enkephalin in the septum were temporally associated with increased hot plate latencies. One day after cessation of dosing with TEL, concentration of 5-HIAA in the caudate nucleus, hippocampus, frontal cortex, and brain stem, and 5-HT in the hippocampus and brain stem were increased. Biogenic amine concentrations were not affected in any other region or at any other time postdosing. A third experiment indicated that TEL-induced analgesia could be attenuated by 10 mg/kg chlordiazepoxide or 10 mg/kg of naloxone. The present results suggest that TEL-induced analgesia may be due to alterations in emotionality or reactivity to noxious stimuli, which may be associated with the alteration in delta opiate mechanism in the limbic system, such as the change of septal enkephalin neuronal activities.

Analgesia↗
PubMed1983

Acrylamide-induced changes in the monoamines and their acid metabolites in different regions of the rat brain.

Acrylamide administration of 10 and 20 mg/kg body weight i.p. in the male rat induced alteration in the levels of dopamine (DA), serotonin (5-HT), and 5-hydroxyindole acetic acid (5-HIAA) in different regions of the brain. Selective but widespread changes were observed in 5-HIAA levels in all regions of the brain studied. 5-HT levels were significantly increased in the brain stem. The DA content also showed a significant increment in the caudate nucleus. These data suggested that the neurotoxicity of acrylamide might be correlated with the overall disturbances of serotonergic system.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1982

Effect of carbon tetrachloride on cardiac lipid peroxidation, serum lipids and enzymes of albino rats.

Carbon tetrachloride (CCl4) at the dose of 0.3 ml/100 g body weight i.p. induced changes after 18 h in the cardiac lipid-peroxidation, serum-free fatty acids (FFA), cholesterol, and enzymes in the rats. The cardiac lipid peroxidation and the activity of serum enzymes GOT and GPT were significantly increased. The levels of serum FFA and cholesterol were significantly decreased.

Alanine Transaminase↗
PubMed1982

Chlordecone (Kepone) exposure in the neonate selectively alters brain and pituitary endorphin levels in prepuberal and adult rats.

It has been reported that the pituitary [Met5]-enkephalin system was regulated by estrogen. Since chlordecone exhibits estrogen-like activity, we explored the possibility that the pituitary level of [Met5]-enkephalin might be altered by this neurotoxicant. A single injection of chlordecone (1 mg/pup on day 4 of age) reduced the level of [Met5]-enkephalin at 70 and 120 days of age in male rats but not in females. Such treatment failed to alter the pituitary levels of beta-endorphin in either sex. However, the same treatment caused a transient reduction in the hypothalamic beta-endorphin level in both male and female rats without affecting the levels of other neuropeptides in the hypothalamus and other brain regions. These results suggest that hypothalamo-pituitary axis may be the primary neural target affected by chlordecone and estrogen-like activity may be related to the chlordecone-elicited decrease in pituitary [Met5]-enkephalin level.

Aging↗
PubMed1982

Subchronic dietary exposure of rats to chlordecone (Kepone) modifies levels of hypothalamic beta-endorphin.

Rats were exposed for extended times to low doses of chlordecone (1 and 6 ppm in the diet). After 105 days of exposure of female rats to this diet, levels of circulating prolactin and growth hormone were not significantly altered, but at the higher dose of chlordecone, hypothalamic beta-endorphin levels were selectively reduced. Since no changes were seen in pituitary levels of beta-endorphin of treated rats, chlordecone had some regional specificity. Levels of dopamine, serotonin, and their metabolites were unchanged in the caudate nucleus of female rats exposed to chlordecone. Thus, low levels of chlordecone appear to selectively affect hypothalamic beta-endorphin suggesting the hypothalamus may be especially sensitive to this neurotoxicant. The gestationally and lactationally-exposed female offspring of these rats showed a major increase in the levels of growth hormone at 100 days of age. However, other parameters assayed remained unaltered. These consisted of biogenic amines within the caudate nucleus, pituitary and hypothalamic met-enkephalin and circulating prolactin, growth hormone, and estrogen.

Animals↗
PubMed1981

Organophosphate pesticide dichlorvos-induced increase in the rate of lipid peroxidation in the different regions of the rat brain: supporting ultrastructural findings.

Commonly used organophosphate pesticide dichlorvos is known to cause neurologic lesions. However, the exact mechanism of its neurotoxicity is, as yet, unclear. Using dose-dependent inhibition of acetylcholinesterase activity as an index of its neurotoxicity, effects of three different doses of dichlorvos (0.6 mg, 1.5 mg, and 3.0 mg/kg body weight i.p. daily for 10 days) have been observed on the rate of lipid-peroxidation in the cerebrum, cerebellum and brain stem of albino rats. Simultaneously, electron microscopic study of the dichlorvos intoxicated rat cerebellum was also carried out. Dose-dependent increase in the rate of lipid peroxidation was found in all the brain regions, and increased incidence of lipofuscin-like pigment granules was discernible in the Purkinie cells of the cerebellar cortex.

Acetylcholinesterase↗
PubMed1981

Regional effects of sulfur dioxide exposure on the guinea pig brain lipids, lipid peroxidation and lipase activity.

Experiments to evaluate the neurochemical action of gaseous pollutants were performed in a specifically designed inhalation chamber. Exposure of guinea pigs to 10 ppm of SO2 for one hour daily for 21 days produced a significant depletion of total lipids and free fatty acids in all brain regions. Phospholipid and cholesterol content of the cerebellum and brain stem were also decreased, but were increased in cerebral hemisphere. Esterified fatty acids were depleted in the cerebral hemisphere and brain stem, but exhibited increment in the cerebellum. The rate of lipid peroxidation and the activity of lipase were increased significantly in all the regions of the brain. The results clearly indicate that SO2-exposure induces degradation of brain lipids. Interestingly, the lipid contents are affected differentially in the various parts of the brain.

Animals↗
PubMed1980

Effects of an organophosphate (dichlorvos) on open field behavior and locomotor activity: correlation with regional brain monoamine levels.

Dichlorvos (O,O-dimethyl-2:2-dichlorovinyl phosphate) was administered IP (3 mg/kg) daily for 10 days to a group of albino rats. Open field behavior was significantly depressed below the mean of the control group. On day 7, ambulation was reduced to 24% of the mean but recovered to 60% on day 10. Similarly, rearing response was decreased on day 7 and showed a fast recovery on day 10 but the preening response further declined on day 10. Defecation, on the contrary, was suppressed to 0% on day 7 and showed complete recovery on day 10. Motor activity showed a significant depression and fine movements were reduced more than gross movements in the second phase. Dopamine was significantly decreased on days 5 and 7 but showed a 13% recovery in the brain stem on day 10. Norepinephrine was significantly reduced in the cerebral hemisphere while serotonin was decreased both in cerebral hemisphere and brain stem. Neither of thse two amines showed significant recovery on day 10. Interesting concordance of the open field behavioral changes with the levels of dopamine, norepinephrine, and serotonin in the various regions of the rat brain was noticeable and has been discussed.

Animals↗
PubMed1979

Organophosphate pesticide DDVP-induced alterations in the rat cerebellum and spinal cord -- an electron microscopic study.

DDVP is an organophosphate pesticide whose neurotoxicity, in the form of cholinesterase inhbition, is well-known. Rats, weighing 200-225 g were given intraperitoneal injections of 3 mg/kg. DDVP daily for 10 days. Following perfusion-fixation, ultrathin sections of the cerebellum and spinal cord were examined with an electron microscope. A large number of electron-dense bodies exhibiting electron-lucid vacuoles were discernible in the perikarya of cerebellar neurons. Aggregations of mitochondria were also seen. Myelin-figures in dendrites and axons of the spinal cord were detected. Evidence of oedema was evident in the spinal cord.

Animals↗