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  • Title: [Changes in cysteine sulfinic acid in rat brain under the experimental elevation of taurine content].
    Author: Tsunoda M.
    Journal: Rinsho Shinkeigaku; 1996 May; 36(5):648-54. PubMed ID: 8905983.
    Abstract:
    Excitatory sulfur amino acids (SAAs) seem to be important, because derangement of SAA metabolism has been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS). Since the concentration of excitatory SAAs in the neural tissue is extremely low, their presence or absence has not been conclusive in the literature. I determined cysteine sulfinic acid (CSA), cysteic acid (CA), homocysteine sulfinic acid (HCSA) and homocysteic acid (HCA) in rat brain by high-performance liquid chromatography using a Shimazu HPLC system LC10. Among the 4 excitatory SAAs mentioned above, the peaks of CA, HCSA and HCA did not appear at the chromatographic retention time corresponding to that of the authentic compounds. Only the peak of CSA was identified by matching retention time with the external standard as well as consistent co-elution with the added authentic compound. Thus the existence of CSA was confirmed and its concentration was 9.18 +/- 3.54 pmol/mg wet weight. Although the other 3 excitatory SAAs were not detected in rat brain, their presence in human brain cannot presently be excluded, because the size of the amino acid pool in rat brain is not the same as that in human brain. I examined in rat brain whether the concentration of CSA would possibly change when taurine, the final product of the metabolic pathway of SAAs, is experimentally increased. The inhalation of nitrous oxide (N2O) and the thyroidectomy have both been known to give rise to the elevation of taurine in the central nervous system, the mechanism of which is reportedly due to the impairment of the folate cycle. The metabolic flow of the SAA pathway is increased as a result of slowing down of the folate cycle, the damage of which has been shown in the brain of N2O-inhaled rats and thyroidectomized rats as well as of patients with ALS. The concentration of CSA was significantly increased in the cerebrum and the brainstem of the N2O-inhaled rats and the thyroidectomized rats, and in the cerebellum of the latter. CSA, recently demonstrated as a neurotransmitter, has been reported to have neurotoxicity stronger than that of gultamate in cultured rat cerebral neurons. The measurement of excitatory SAAs, especially CSA in nervous tissue of ALS will be required, although relevance of excitatory SAAs to the pathogenesis of ALS is not certain at present.
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