Effects of anticonvulsant drugs on chromosomes.

Roman, Iza; Caratzali, A

doi:10.1136/bmj.4.5781.234-b

Cited by 18 publications

(3 citation statements)

References 4 publications

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“…PHT has been found mutagenic in male germ cells of Swiss mice (Ramaniah et al, 1980). It has also been linked to an increase in chromosomal aberrations in bone marrow cells of rats (Roman and Caratzalli, 1971) and in human peripheral leukocyte cultures in vivo (Grosse et al, 1972;Herha and Obe, 1976) and in vitro (Muniz et al, 1%9; Welzel and Gamer, 1975).…”

mentioning

confidence: 99%

Lack of Sister Chromatid Exchange Induction in Phenytoin‐Treated Patients with Epilepsy

Schaumann¹,

Winge²,

Garry

1989

Epilepsia

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Phenytoin (PHT) has been suspected of having a mutagenic effect with chronic administration, but the existing evidence is equivocal. Contradictory results have been obtained using different testing systems. Sister chromatid exchange (SCE), a sensitive indicator of genotoxic environmental influences, has been used in only a few limited studies of PHT users, with varying results. The present study was designed to evaluate the potential mutagenicity of PHT in a more objective and reliable way than has been done previously. Following careful screening procedures, 16 adult male patients with epilepsy receiving long-term PHT monotherapy and 16 healthy controls were selected for a study of SCE frequencies in peripheral lymphocytes. The patients and controls were matched for sex, age, and smoking habits. Strict exclusionary criteria were observed, including all factors known to affect or suspected of affecting the SCE frequencies. Statistical analyses did not reveal any significant differences between the SCE rates of PHT-treated patients and controls, indicating a lack of PHT mutagenicity as expressed by induction of SCE in adults.

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confidence: 99%

Lack of Sister Chromatid Exchange Induction in Phenytoin‐Treated Patients with Epilepsy

Schaumann¹,

Winge²,

Garry

1989

Epilepsia

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“…Br</>gger [2] described that the therapeutic dose of ethotoin did not cause chromosome abnormality. Roman and Caratzali [17] recognized high-level abnormal metaphase in bone marrow cells of rats treated with phenytoin, and this anomaly recovered to the normal level 7 days after withdrawal, mentioning the relevance between chromosome abnormality and folic acid synthesis inhibit ing the action induced by anticonvulsant drugs. As a common chromosome ab normality appearing in users of anticonvulsant drugs,Mdrquez-Monter et al [9] described numerous abnormalities such as tetraploidy or hypotetraploidy, but there were other reports which insisted on the increase of breaks [14] or exchange-type abnormalities [6].…”

Section: Discussionmentioning

confidence: 99%

Effects of Long-Term Administration of Anticonvulsant Drugs on Chromosomes in Man

Matsushima¹,

Hazama²,

Kawahara³

1981

Int Pharmacopsychiatry

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Effects of long-term administration of anticonvulsant drugs on chromosomes in epileptic mothers and their children were examined. Specimens from peripheral lymphocytes were prepared by incubation for 3 days and colchicine treatment. Results obtained were as follows: (1) The incidence of abnormal cells in the epileptic mother group over 9 years of drug administration was significantly higher than in the group below 9 years. (2) Most of chromosome abnormalities found in subjects were of comparatively simple morphological aberrations such as gaps or breaks. The incidence of the chromosome-type abnormalities was significantly higher in the patient group than in the control group. (3) Chromosome abnormality of children showed a positive correlation with that of mothers but was not significant. (4) The incidence of chromosome abnormality in children was reduced along with aging. (5) These observations could be interpreted to suggest that chromosome abnormality appearing in children born from epileptic mothers under drug therapy was probably formed by direct effects of anticonvulsant drugs on the fetal hematopoietic system.

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“…Both folic acid and vitamin B,* are essential in the synthesis of deoxyribonucleic acid, and their reduced levels may be among the factors predisposing to chromosome damage (Heath, 1966). It has been suggested (Roman and Caratzali, 1971) that the chromosome abnormalities induced by anticonvulsant drugs may be due to the inhibition of the synthesis of either folic acid or proteins constituting the chromosome matrix. Recently, folic acid deficiency was implicated in inducing the expression of chromosome fragile sites (Yunis and Soreng, 1984).…”

Section: In Vitromentioning

confidence: 99%

Effects of Carbamazepine on Human Chromosomes

et al. 1985

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The effect of carbamazepine (CBZ) on human chromosomes was studied in an effort to determine its mutagenic potential. Analysis of chromosome breakage, sister chromatid exchanges (SCE), and cell cycle studies were performed in peripheral lymphocyte cultures. The in vivo studies failed to detect any significant increase of chromosome aberrations or SCE or any slowing of the cell cycle. A significant dose-dependent increase in chromosome aberrations but not in SCE was observed in the in vitro analyses. No correlation was observed between chromosome breaks and SCE in either the in vivo or in vitro studies. The negative in vivo results indicate an absence of detectable chromosome-damaging effects of CBZ used in monotherapy in human subjects.

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Effects of anticonvulsant drugs on chromosomes.

Cited by 18 publications

References 4 publications

Lack of Sister Chromatid Exchange Induction in Phenytoin‐Treated Patients with Epilepsy

Lack of Sister Chromatid Exchange Induction in Phenytoin‐Treated Patients with Epilepsy

Effects of Long-Term Administration of Anticonvulsant Drugs on Chromosomes in Man

Effects of Carbamazepine on Human Chromosomes

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