Publications by authors named "V B Winge"

The potential of the widely prescribed antiepileptic drugs (AEDs) phenytoin (PHT) and phenobarbital (PB) to interact with genetic material was tested using sister chromatid exchange (SCE) assay. Thirty adult male patients with epilepsy receiving long-term AED therapy (16 with PHT, 6 with PB, and 8 with combined PHT and PB therapy) and 30 healthy controls were selected for the study of SCE frequencies in peripheral lymphocytes. The patients and controls were carefully screened and matched for sex, age, and smoking habits.

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We investigated the effect of the antiviral drug amantadine (AmTd) on polyclonal activation of thymic-dependent (T) and thymic-independent (B) lymphocytes from normal mice. In the present studies, T-lymphocytes are defined by their response to concanavalin A (Con A) and B-lymphocytes by their response to lipopolysaccharide (LPS). Polyclonal activator-induced lymphocyte proliferation was assessed by quantifying cellular incorporation of tritiated thymidine.

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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.

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Sister chromatid exchanges (SCE) were studied in peripheral lymphocyte cultures of 13 adult male patients with epilepsy treated chronically with valproate (VPA) and in their matched controls. No statistically significant differences in SCE level were found between the patient and control groups, indicating a lack of mutagenic potential of VPA within the therapeutic dose range.

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The potential of phenobarbital to interact with DNA has been studied using the sister chromatid exchange (SCE) assay in peripheral lymphocytes of nine adult male patients with epilepsy and of their matched controls. All patients were otherwise healthy individuals, treated chronically with phenobarbital in monotherapy. No statistically significant differences in SCE levels were found between the patient and control groups.

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