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At least 19 recordsLinked to original sources

PubMed1986

N-[11C-Methyl]chlorphentermine and N,N-[11C-dimethyl]chlorphentermine as brain blood-flow agents for positron emission tomography.

N-[11C-methyl]chlorphentermine ([11C]NMCP) and N,N-[11C-dimethyl]chlorphentermine ([11C]NDMCP) were prepared from chlorphentermine and 11CH3I in DMF and evaluated in rats as brain blood-flow agents for positron emission tomography (PET). Tissue distribution of [11C]NMCP showed that brain uptake was 2.70 +/- 0.40% of injected dose per organ at 5 min with no change in radioactivity concentration up to 30 min after i.v. injection. Approximately 80% of the initial brain uptake remained at 60 min. On the other hand, initial brain uptake of [11C] NDMCP (3.66 +/- 0.31 and 3.63 +/- 0.88% injected dose per organ at 5 and 15 min, respectively) was greater than that of [11C]NMCP. The brain activity however, rapidly decreased to 2.38 +/- 0.17 and 1.82 +/- 0.32% at 30 and 60 min, respectively. Because of its longer retention in the brain compared with [11C]NDMCP, [11C]NMCP would be a potential brain blood-flow agent for quantitative PET studies.

Animals↗

PubMed1984

Effect of chlorphentermine pretreatment on the distribution of chlorphentermine in isolated perfused rat lungs.

Previous studies have shown that a 7-day treatment of rats with chlorphentermine (CP) enhances total pulmonary phospholipids and significantly enhances the accumulation of CP in perfused lungs. This study was conducted to determine if the accumulation of CP was associated with a particular fraction of the lung, and if the enhanced uptake correlated with the increased phospholipids. Rats were treated daily for 7 days with 50 mg/kg CP dissolved in saline and pair-fed controls received the vehicle only. On Day 8, the rats were sacrificed, and the lungs were removed, ventilated, and perfused. [14C]Chlorphentermine (5 mumol) was added to the perfusate of control and CP-pretreated lungs. After perfusion, the lung was homogenized and subjected to standard fractionation procedures. Some lungs were examined by light and electron microscopy. After 60 min of perfusion, CP uptake by lungs obtained from CP-treated rats was enhanced in comparison to uptake by lungs from control rats. However, CP was distributed uniformly among subcellular fractions, and CP pretreatment did not alter this pattern. Pulmonary macrophages obtained from CP-treated animals contained 8 times more CP than controls. Increased CP uptake following pretreatment can be accounted for by increased CP in the macrophages of treated rats. Macrophages in the lung tissue and in the lavage fluid from rats treated with CP were more numerous and larger than in controls lungs. This suggests that a close association may be found between accumulated CP and macrophage uptake.

Animals↗

PubMedDate not supplied

Effect of chlorphentermine pretreatment on chlorphentermine uptake by isolated perfused rat lung.

Chlorphentermine (CP), an anorectic agent currently in use, is known to be highly accumulated in the lung, causes pulmonary phospholipidosis, and has been suspected of causing pulmonary hypertension. These studies were undertaken to characterize the uptake and accumulation processes and to examine the effect of subacute CP treatment on the uptake kinetics of CP in the rat lung. Animals were treated po with a saline solution of CP (50 mg/kg/day) for 7 days and the controls received the vehicle only. Artificially ventilated isolated rat lung preparations were perfused with Krebs-Ringer bicarbonate buffer containing bovine serum albumin. CP was not metabolized by control or pretreated perfused lungs or by their 9000g supernatant or microsomal fractions. In recirculating perfusion experiments, steady-state uptake was reached after 20 min of perfusion with 0.17 mM CP. Lungs from rats treated with CP as described above accumulated CP to a greater extent and more rapidly than did lungs from control rats. Similarly, lungs from rats treated with CP accumulated significantly greater quantities of CP than control lungs during single-pass perfusion experiments. Whereas control lungs reached a steady state uptake within 7 min, lungs from CP treated animals failed to reach a steady-state uptake during a 10-min perfusion. The lungs from CP-treated rats retained most of the accumulated CP and exhibited a significantly increased half life of efflux in comparison to control rats. Removal of Na+ from the perfusion medium or the addition of harmaline significantly decreased the half-life of CP uptake and the amount of CP accumulated by the lung.

Absorption↗

PubMed1988

Association of chlorphentermine with phospholipids in rat alveolar lavage materials, alveolar macrophages and type II cells.

Administration of chlorphentermine to rats leads to an increase in the phospholipid content of pulmonary surfactant materials and alveolar macrophages. It is known that this drug binds to pure phospholipids and prevents their degradation by phospholipases. Therefore, experiments were carried out to determine if chlorphentermine binds to surfactant phospholipids in vitro and to measure the in vivo association of drug with phospholipids in alveolar lavage materials from rats injected with [14C]chlorphentermine. The presence of chlorphentermine in alveolar macrophages, type II cells and other small pneumocytes (a population of lung cells which does not include alveolar macrophages or type II cells) from treated animals was also assessed. Binding of the drug to surfactant phospholipids, as measured with the fluorescent probe, 1-anilino-8-naphthalene sulfonate, occurs in vitro and does not differ in various subfractions of alveolar lavage materials isolated by differential centrifugation. Following daily administration of chlorphentermine to rats for 3 days, the drug appears to be associated with surfactant phospholipids such that the molar ratio is 1:100 (chlorphentermine/phospholipid). Chlorphentermine is also associated with alveolar macrophages (molar ratio, 1:18) and type II cells (molar ratio, 1:33). Not much drug is associated with the population of other lung cells (molar ratio, 1:333). In alveolar macrophages, approx. 70% of the drug seems to be bound to phospholipid and/or sequestered in subcellular organelles. However, only 20% of the chlorphentermine is bound and/or sequestered in type II cells. The results of these experiments suggest that following chlorphentermine administration, the drug is associated with phospholipids in acellular pulmonary lavage materials, alveolar macrophages and type II cells. This drug-phospholipid interaction may impair phospholipid degradation and lead to a phospholipidosis in surfactant materials and alveolar macrophages.

Animals↗

PubMed1983

Chlorphentermine-induced alterations in pulmonary phospholipid content in rats.

Daily, intraperitoneal administration of the anorectic drug chlorphentermine (30 mg/kg) for 5 days to rats significantly increased phosphatidylcholine and total phospholipid content after 1 week and reached a maximal level 4 weeks after treatment in whole lung tissue (unlavaged lungs) and in sessile tissue in which alveolar lipids and macrophages were removed by pulmonary lavage (lavaged lungs). In lavaged lung, a significant rise in the content of sphingomyelin, phosphatidylserine plus phosphatidylinositol component, and phosphatidylethanolamine plus phosphatidylglycerol fraction occurred after 2 weeks, remained at this increased level for 4 weeks, and was followed by a return to control amounts after 5 weeks. In unlavaged lung, the chlorphentermine-induced elevation in sphingomyelin content seen after 1 week persisted at this same significant level even 5 weeks after treatment. Regardless of experimental duration, pulmonary glycogen levels were not altered markedly by chlorphentermine in unlavaged or lavaged tissue. Phenobarbital (30 mg/kg) did not markedly alter pulmonary glycogen and phospholipid component levels. Simultaneous phenobarbital and anorectic drug administration prevented the chlorphentermine-induced rise in total phospholipid, sphingomyelin, and phosphatidylcholine in unlavaged lung without a change in glycogen. A 7-day withdrawal from chlorphentermine treatment in rats previously injected with drug for 2 weeks resulted in a return to control in the levels of sphingomyelin, phosphatidylcholine, and total phospholipid in unlavaged lung. Extension of withdrawal from treatment for 2 weeks produced a significant decrease in all phospholipid components below control values, suggesting that a possible imbalance in synthetic and catabolic activity may persist after drug removal. The concentration of lung glycogen was not altered significantly by chlorphentermine treatment or withdrawal from drug administration. Our results indicate that the chlorphentermine-induced rise in phospholipid components was time-dependent in lavaged and unlavaged lungs, and the increase in phosphatidylcholine occurred independently of a change in glycogen. In addition, the present study shows that the chlorphentermine-induced changes in phospholipid levels are reversible and almost completely prevented by phenobarbital.

Animals↗

PubMed1986

Mitochondrial alterations in the brain of the rat caused by chlorphentermine.

The effects of chlorphentermine on the bioenergetics and activity of monoamine oxidase in mitochondria from the brain of the rat were examined. Oxidation rates of glutamate and succinate were investigated in the presence of chlorphentermine (0.1-5.0 mM). In small concentrations (0.1-1.0 mM), chlorphentermine decreased the respiratory control ratio and the adenosine diphosphate oxygen (ADP/O) ratio, and stimulated state four respiration. State three respiration and the uncoupled state were also decreased, but to a lesser degree. In the presence of larger concentrations of chlorphentermine (1.0-5.0 mM), the respiration in states four, three, and in the uncoupled state, as well as the respiratory control ratio and ADP/O ratio, were decreased significantly. These data indicate that chlorphentermine functions as an uncoupler of oxidative phosphorylation. Oxidation of norepinephrine, serotonin, octopamine, tyramine and dopamine by monoamine oxidase (MAO), an enzyme marker of the outer mitochondrial membrane, was inhibited in the presence of 0.01 to 0.1 mM of chlorphentermine. Oxidation of tryptamine and benzylamine was unaffected. A kinetic study of the oxidation of serotonin in the absence and presence of chlorphentermine (0.025-0.1 mM) indicated that both the Vmax and Km were affected. This drug is an inhibitor of monoamine oxidase of mitochondria of the brain with mixed type inhibition. These combined data show that chlorphentermine affects biochemical processes in both inner and outer mitochondrial membranes.

Animals↗

PubMedDate not supplied

Modification by phenobarbital of chlorphentermine-induced changes in lung morphology and drug-metabolizing enzymes in newborn rats.

Treatment of newborn rat pups with 60 mg/kg.d chlorphentermine for 7 d produced on accumulation of alveolar foam cells accompanied by an increase in relative pulmonary tissue weight. In contrast, administration of 20 mg/kg.d for 1 wk did not markedly alter lung ultrastructure or weight in newborns. Both doses of chlorphentermine elevated the activity of pulmonary aminopyrine N-demethylase but not that of aniline hydroxylase. The increase in relative liver weight was associated with stimulation of the activities of aniline hydroxylase and aminopyrine N-demethylase in newborns administered either chlorphentermine dose. Phenobarbital treatment produced an increase in relative liver weight accompanied by elevated activities of pulmonary aminopyrine N-demethylase and hepatic aniline hydroxylase and aminopyrine N-demethylase. Simultaneous barbiturate and chlorphentermine administration produced stimulation in liver enzymes to the same extent as phenobarbital alone. In contrast, phenobarbital potentiated the chlorphentermine-induced rise in pulmonary aminopyrine N-demethylase. In the case of 60 mg/kg chlorphentermine and barbiturate, the observed potentiation of lung enzyme activity was associated with a reduction in the number of alveolar foam cells. The results suggest that chlorphentermine and phenobarbital stimulate drug-metabolizing enzyme in lung and liver of newborn rats and that phenobarbital may provide protection against phospholipidosis through stimulation of pulmonary, drug-metabolizing enzymes.

Aminopyrine N-Demethylase↗

PubMed2000

The effect of fenfluramine on the pulmonary disposition of 5-hydroxytryptamine in the isolated perfused rat lung: a comparison with chlorphentermine.

A possible mechanism for fenfluramine-induced pulmonary hypertension has been investigated. Fenfluramine, like chlorphentermine, may inhibit the pulmonary uptake and/or metabolism of 5-hydroxytryptamine (5-HT). This allows more 5-HT to remain in the pulmonary circulation, where it may exert a greater vasoconstrictor action resulting in pulmonary hypertension. Chlorphentermine has been shown to inhibit the uptake and metabolism of 5-HT. The effect of fenfluramine on the pulmonary disposition of [14C]5-HT has been investigated, in comparison with chlorphentermine, using a recirculating isolated perfused rat lung system. The pulmonary disposition of [14C]5-HT was assessed by measuring the change in [14C]5-HT concentration in the perfusion medium during the experiment and at the end, and the concentration in the lung at the end of the experiment. The concentration of 5-hydroxyindoleacetic acid, a metabolite of 5-HT, was measured in perfusate and lung samples. Mean pulmonary clearance of 5-HT for the control lung and lungs challenged with either fenfluramine (2.5 microM) or chlorphentermine (25 microM) was 4.514, 1.316 and 1.007 mL min(-1), respectively (n = 5). The concentration of 5-HT found in the lungs at the end of the experiment for the control and the lungs preloaded with fenfluramine or chlorphentermine was 695.05+/-9.69, 638.65+/-10.27 and 617.3+/-14.38 ng g(-1), respectively. Fenfluramine, like chlorphentermine, inhibited the pulmonary disposition of 5-HT resulting in an elevated perfusate level of 5-HT. This is a possible contributing mechanism for fenfluramine-induced pulmonary hypertension. The effect of fenfluramine was less pronounced than chlorphentermine.

Animals↗

PubMed1986

Alterations in rat alveolar surfactant phospholipids and proteins induced by administration of chlorphentermine.

Chlorphentermine is a cationic amphiphilic drug which produces a phospholipid storage disorder in rat lungs. Experiments were carried out to characterize changes in the composition of acellular alveolar lavage materials and to study possible mechanisms by which pulmonary surfactant phospholipidosis is produced by administration of the drug. Following ten daily injections of chlorphentermine (25 mg/kg body weight), there are 12.2- and 13.6-fold increases of pulmonary lavage total phospholipids and disaturated phosphatidylcholines (disaturated PC), respectively. In addition, there is a 2.8-fold increase in total protein and a 12.7-fold increase in the surfactant apoprotein group with molecular weights from 28,000 to 32,000. We measured incorporation of labeled palmitate, choline and glycerol into disaturated PC in type II cells and alveolar macrophages isolated from control and chlorphentermine-treated animals. The drug does not affect the incorporation of labeled substrates into disaturated PC in either cell type. However, in alveolar macrophages there is a decrease in the rate of intracellular degradation of recently synthesized disaturated PC in chlorphentermine-treated animals. The drug also inhibits the phospholipase-induced catabolism of rat surfactant disaturated PC which occurs during incubation of alveolar lavage fluid in vitro at 37 degrees C. When the lavage fluid is divided into subfractions by differential centrifugation, a larger percentage of the phospholipid is distributed in the less sedimentable subfractions in chlorphentermine-treated animals relative to controls, suggesting the accumulation of older surfactant materials. These results suggest that chlorphentermine-induced phospholipidosis of pulmonary surfactant materials is due to decreased rates of phospholipid degradation.

Animals↗

PubMed1985

Gentamicin or chlorphentermine induction of phospholipidosis in the developing organism: role of tissue and species in manifestation of toxicity.

Daily, s.c. injection of gentamicin (100 mg/kg) for 2 days produced a significant increase in total phospholipid content of newborn rat kidney. Separation of individual phospholipid components revealed a significant rise in renal phosphatidylserine, phosphatidylinositol and phosphatidylcholine, whereas no marked change was noted in sphingomyelin, phosphatidylethanolamine or phosphatidylglycerol. Gentamicin did not significantly alter individual phospholipid classes and total phospholipid content in newborn rat liver and lung. Daily, oral chlorphentermine (60 mg/kg) administration also elevated total renal phospholipid levels and all individual phospholipid classes except sphingomyelin. In addition, a significant rise in all phospholipid components and total phospholipid content was noted in lungs of chlorphentermine-treated newborns. In the case of rat kidney, both gentamicin and chlorphentermine produced the greatest percentage of increase in phosphatidylinositol, whereas in lung phosphatidylcholine exhibited the highest percentage of elevation in response to chlorphentermine. In newborn rat liver, chlorphentermine did not induce alterations in individual and total phospholipid content. Gentamicin or chlorphentermine (1 mg/egg) failed to induce a phospholipidosis in chick embryo kidney and liver. Evidence suggests that drug-induced phospholipidosis is both species- and tissue-dependent and that this metabolic phenomenon is associated with inhibition of lysosomal phospholipases.

Animals↗

PubMed1987

Cationic amphiphilic drug-induced renal cortical lysosomal phospholipidosis: an in vivo comparative study with gentamicin and chlorphentermine.

Daily subcutaneous injection of gentamicin (100 mg/kg) for 2 days produced a significant decrease in the activities of alkaline phosphatase, a brush-border membrane marker, and Na+-K+ ATPase, a basolateral membrane marker, in adult rat kidney cortex. Analysis of homogenate and lysosomal fractions revealed a significant rise in the concentration of total renal cortical phospholipid, phosphatidylserine, phosphatidylcholine, and phosphatidylinositol. In the lysosomal fraction, an increase in the levels of phosphatidylglycerol and phosphatidylethanolamine was also noted. Daily, oral chlorphentermine (60 mg/kg) administration for 5 days significantly reduced renal Na+-K+ ATPase without a marked change in alkaline phosphatase. As in the case of gentamicin, chlorphentermine produced a significant elevation in phosphatidylserine, phosphatidylcholine, and phosphatidylinositol as well as total phospholipid in both the homogenate and lysosomal fractions of kidney cortex. The observed chlorphentermine- or gentamicin-induced renal phospholipidosis was associated with a significant reduction in the activity of phosphatidylinositol-specific phospholipase C. The drug-induced inhibition of phospholipase C was quantitatively equal in the renal cortical homogenate and lysosomal fractions. In addition, gentamicin significantly inhibited the activity of phosphatidylserine-phospholipase C and phosphatidylcholine-phospholipase C in renal cortical homogenate. In contrast, only the activity of phosphatidylinositol-specific phospholipase C was decreased in chlorphentermine-treated kidneys. Evidence thus indicates that the gentamicin-induced accumulation of phospholipid in renal cortical lysosomes is associated with inhibition of various forms of phospholipase C, while in the case of chlorphentermine the inhibition of different phospholipases may be involved in phospholipid accumulation.

Animals↗

PubMed1982

Neonatal toxicity in rats following in utero exposure to chlorphentermine or phentermine.

The administration of chlorphentermine (30 mg/kg) to pregnant rats during the last 5 days of gestation resulted in the development of a phospholipidosis in the lungs of the dams. The disorder developed in utero, as the phospholipidosis was evident in the lungs of the neonates when examined at 12 h postpartum. In contrast, a phospholipidosis was not observed in the lungs of the dams or neonates following phentermine treatment (30 mg/kg). Concurrently, neonates of the chlorphentermine-treated dams displayed a significant decrease in body weight in comparison to controls. Between 16 h and 24 h postpartum, 83% of the neonates of chlorphentermine-treated dams died. Cross-fostering and starvation experiments revealed that the lethality was not due to aberrant maternal behavior by the chlorphentermine-treated dams or malnutrition of the neonates. Histological examinations revealed endothelial and septal alterations in the lungs of neonates from chlorphentermine-treated dams. No signs of toxicity, as evidenced by the maintenance of body weight, or lethality were observed in the neonates of the phentermine-treated dams.

Animals↗

PubMed1976

Effect of chlorphentermine on the lipids of rat lungs.

Chronic administration of chlorphentermine to rats resulted in a reduction of body weight compared to a normal control group. The weight of the heart, liver, kidney, and spleen was less in the treated group while the weight of the lungs was increased significantly. There was no change in the ratio of right ventricular to left ventricular weight in the rats treated with chlorphentermine, supporting the views that this drug does not cause pulmonary hypertension. Biochemical analysis showed that the increase in the weight of the lungs was due to the accumulation of phospholipid. All classes of phospholipid were affected, but particularly phosphatidyl choline, the tissue concentration of which increased nine times. Chlorphentermine also increased the proportion of palmitate present in pulmonary phosphatidyl choline. Histological examination of the lung after treatment with chlorphentermine showed evidence of this drug-induced lipidosis. No conclusion can as yet be reached as to the mechanism involved in the accumulation of phospholipid in the lung after chlorphentermine.

Animals↗

PubMed1976

Palmitic acid-1-14C incorporation and turnover in lung phospholipids of rats treated with chlorphentermine, RMI 10.393 and Ro 4-4318.

The effects of 3 lipidosis-inducing drugs on the incorporation and turnover of palmitic acid-1-14C in lung phospholipids was studied. In rats treated with 1 dose of chlorphentermine or RMI 10.393, the incorporation of palmitate-1-14C into most lung phospholipid fractions was moderately decreased, but markedly lowered after 1 dose of Ro 4-4318. Eight doses of chlorphentermine and RMI 10.393 strongly inhibited the incorporation of palmitate-1-14C into lung phospholipids, whereas with 8 doses of Ro 4-4318 the incorporation was highly increased. Thirty hours after the last of 3 injections of the labeled palmitic acid the turnover of most lung phospholipids was considerably lower in chlorphentermine- and RMI 10.393-treated rats than in controls. Ro 4-4318, however, induced a highly increased turnover of most phospholipids. After 54 h, this effect had practically disappeared. Our studies showed that phospholipid storage after treatment with chlorphentermine and RMI 10.393 is mainly due to decreased degradation of phospholipids, whereas increased synthesis accounts for the effect of Ro 4-4318.

Amitriptyline↗

PubMedDate not supplied

Impairment in pulmonary bioenergetics following chlorphentermine administration to rats.

Biochemical alteration in pulmonary oxidative metabolism and morphological integrity of lung mitochondria were examined in rats following administration of chlorphentermine (30 mg/kg, ip, 5 days per week) for 1 or 2 weeks. During the first week of treatment, body weight gain and food intake were decreased markedly but returned to control levels during the second week. Phospholipid content of the lung was increased 31% and 110% after 1 and 2 weeks of treatment, respectively. This was accompanied by a striking intraalveolar accumulation of hypertrophic alveolar macrophages. The metabolism of both (1-14C)- and (6-14C)-glucose was decreased 27% and 26%, respectively, after 2 weeks of drug treatment. In rat lung mitochondria, chlorphentermine significantly lowered the RCR and ADP/O ratio and stimulated state 4 respiration. State 3 respiration and uncoupled state respiration were unaffected. These data indicate that chlorphentermine functions as a true uncoupler of oxidative phosphorylation when administered in vivo. Furthermore, disruption of mitochondrial membranes was observed frequently in lung mitochondria from treated animals. These combined data indicate that the induction of pulmonary phospholipidosis by chlorphentermine is accompanied by marked alterations in subcellular bioenergetics and mitochondrial structure.

Animals↗

PubMed1981

Modification by hyperoxia of chlorphentermine- or phentermine- induced effects on newborn rat lung morphology and metabolism.

Treatment of newborns with 20 mg/kg/day chlorphentermine orally for 1 week increased incorporation of thymidine into lung DNA without an associated change in tissue morphology or cyclic AMP levels. An increase in chlorphentermine dose to 60 mg/kg resulted in an accumulation of alveolar hypertrophic macrophages and a rise in incorporation of thymidine into lung DNA; however, cyclic AMP levels were decreased. In contrast, 20 or 60 mg/kg/day for 1 week phentermine-induced depression in the incorporation of thymidine into pulmonary DNA was accompanied by a decrease in cyclic AMP but no apparent alteration in tissue morphology. Hyperoxia did not modify the phentermine-induced changes in cyclic AMP levels and pulmonary ultrastructure. In contrast, hyperoxia altered the responsiveness of newborns to 20 mg/kg chlorphentermine as evidenced by the presence of foam cells. Data suggest that the chlorphentermine-induced increase in DNA synthesis in newborn lung seems independent of changes in cyclic AMP and tha modification of drug-induced alterations by hyperoxia may be related to the chemical structure of a compound.

Animals↗

PubMed1988

Role of phospholipase C in chlorphentermine-induced pulmonary phospholipidosis in rat.

Daily, oral administration of chlorphentermine (60 mg/kg) for 5 days to rats produced a significant increase in the concentration of whole lung total phospholipid as well as sphingomyelin, phosphatidylserine, phosphatidylethanolamine, phosphatidylglycerol, phosphatidylinositol, and phosphatidylcholine. Similarly, a significant elevation in total and all individual phospholipid components was found in the lysosomal fraction of chlorphentermine-treated rat lung. In contrast, the activities of pulmonary Na+,K+-ATPase and alkaline phosphatase, enzymatic markers of membrane function, were not markedly affected by chlorphentermine treatment. The observed lung phospholipidosis was accompanied by inhibition of phospholipase C activity. Regardless of the phospholipid substrate, chlorphentermine significantly decreased pulmonary phospholipase C to approximately the same extent. Our data show that accumulation of phospholipid in whole lung and lysosomes is associated with an inhibition of phospholipase C activity.

Alkaline Phosphatase↗

PubMed1994

Chlorphentermine-induced lipidosis in the rat retina: a functional and morphological study.

Chronic administration of the cationic amphiphilic anorexigenic drug chlorphentermine to rats has previously been shown to induce extraocular and ocular lipidosis: large numbers of lipidosis-related cytoplasmic inclusions can be found in the pigment epithelium and smaller numbers in the neuroretina. In the present study, female albino Wistar rats were treated orally with chlorphentermine (30-45 mg/kg body weight) for 4-16 weeks. The animals were submitted to electroretinography, and the retinae were prepared for histological investigations. Our histological findings corresponded to previous reports. The changes in electroretinographic parameters were low. The clearest change was a reduction of the b-wave amplitude of 20% after 12 and 16 weeks of treatment compared with the values before drug treatment. The a-wave amplitude did not differ from that in the control group. Lipidosis in the neuroretina may be the reason for functional influences on the b-wave amplitude. The function of the receptor cells, which is represented by the a-wave, appeared unaffected by chlorphentermine.

Administration, Oral↗