Taurine transport in epilepsy.

Abstract

Previous studies of plasma taurine concentrations in epileptics have yielded equivocal results. We measured plasma and urinary taurine in 41 epileptic and 68 control subjects and found plasma concentrations among epileptics to be comparable in general to those of controls, but that two or three classes of plasma taurine concentrations, possibly genetically regulated, occur in both epileptic and control subjects. Our previous studies and data from the present study on taurine excretion revealed three excretion classes under genetic control. The principal finding is that epileptics include disproportionate numbers of low excretors (high reabsorbers), who are presumptive homozygotes for the allele effecting higher reabsorption. If confirmed, these findings suggest that the transport of taurine, rather than absolute taurine concentration, may explain the efficacy of taurine administration in some epileptics but not in others. The locus involved may be one component in the polygenic diathesis to the idiopathic epilepsies.

Platelet taurine content in Friedreich's disease

“…In this they resemble subjects with muscular dystrophy (Lemieux et al, 1984, this issue). The extent of taurine handling appears to follow a genetic pattern (Barbeau et al, 1982), as described in other entities and normal control subjects by Goodman et al (1980). The concentration of taurine in the cerebrospinal fluid is normal (Lemieux et al, 1978), but it is slightly elevated in the cerebellum (Huxtable et al, 1979) in Friedreich's disease.…”

“…3.73 ± 0.87 0.04 ± 0.02 0.04 + 0.03 0.37 ±0.14 0.13 ±0.07 0.25 + 0.10 0.08 ± 0.03 (Huang et al, 1980;Yorek et al, 1984), by genetics (Goodman et al, 1980) or by a deficit in pantothenic acid which is known to increase taurine excretion (Koyanagi and Obori, 1965) or by all these changes, is still to be decided by further studies. The end result, however, is that Friedreich's disease patient may not have available, at the proper place and at the proper time, the quantity of extra taurine required to dampen the metabolic and osmotic effects of these stresses, despite the fact that tissue taurine concentrations (at metabolic rest) are normal.…”

The Quebec Cooperative Study of Friedreich's Ataxia: 1974-1984 — 10 Years of Research

“…In both these traits they resemble subjects with muscular dystrophy (VI-19). The extent of taurine handling appears to follow a genetic pattern (V-23), as described in other entities and normal control subjects by Goodman et al (1980). The concentration of taurine in the cerebrospinal fluid is normal (11-13), but it is slightly elevated in the cerebellum (111-20) in Friedreich's disease.…”

Studies on the role of taurine in Friedreich's ataxia

“…The dose of taurine used was strictly 4 mg/kg. As shown by Goodman and his collaborators, this dose produces the greatest difference between genotypes (Conolly and Connolly et al, 1979;Goodman et al, 1980;Goodman and Connolly, 1982). The test was started between 8 and 9 am, after an overnight fast.…”