α‐Guanidinoglutaric Acid in Cobalt‐Induced Epileptogenic Cerebral Cortex of Cats

Mori, Akitane; Akagi, Masayuki; Katayama, Yukitoshi; Watanabe, Yozo

doi:10.1111/j.1471-4159.1980.tb03697.x

Cited by 38 publications

(9 citation statements)

References 12 publications

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“…In other studies, the levels of some endogenous guanidino compounds increased in the focal cobalt epilepsy model of cats, i.e. tx-guanidinoglutaric acid increased not only in the ipsilateral but also in contralateral cerebral cortex after unilateral cobalt placement (13). We also observed a two-to three-fold increase in GAA and MG levels in the cerebral cortex and hippocampus (2) months after ferric chloride injection into the sentory motor cortex, inducing an epileptic focus (14).…”

Section: Introductionsupporting

confidence: 60%

Guanidino compounds generate reactive oxygen species

et al. 1996

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SUMMARYMethylguanidine, guanidinoacetic acid and guanidinosuccinic acid are endogenous substances in body tissues. Extremely high levels of these substances are known to be related to the pathogenesis of epilepsy and renal failure such as uremia. In this study it was demonstrated that methylguanidine, guanidinoacetic acid and guanidinosuccinic acid, and arginine generate hydroxyl radicals in aqueous solution. These findings suggest that a high level of guanidino compounds accumulating near or within cells such as neurons (in an epileptogenic focus) or nephrons (in uremic patients) may cause free radical damage leading to these clinical disorders. Arginine may have a similar role in the pathogenesis of hyperarginemia.

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Section: Introductionsupporting

confidence: 60%

Guanidino compounds generate reactive oxygen species

et al. 1996

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“…The abundance of guanidocontaining substances in the spinal fluid and in the CNS (guanido acetic acid, guanido glutaric acid, guanido succinic acid, etc.) [12], as well as the existence of a structure-activity relationship for imidazoline structure in the NRL at the medulla …”

mentioning

confidence: 98%

Isolation of an endogenous clonidine‐displacing substance from rat brain

Atlas

Burstein

1984

FEBS Letters

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An endogenous substance which specifically displaces clonidine, yohimbine and rauwolscine from rat brain cyz-adrenergic receptors, has been isolated. The new compound, designed clonidine-displacingsubstance (CDS), has been partially purified by ion exchange chromatography, zone electrophoresis and high performance liquid chromatography (HPLC). CDS binds specifically to cYz-adrenergic receptors by competing with either cuz-adrenergic agonists or cYz-antagonists, but has no effect on the specific binding of [3H]prazosin to cYr-adrenergic receptors in rat brain membranes. In the course of isolation, CDS was shown to be neither the endogenous neurotransmitter (-)norepinephrine (NE) nor the guanyl nucleotide GTP which lowers the specific binding of cYz-agonists to the cus-adrenergic receptors. Clonidine cYrAdrenergic receptor Yohimbine

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“…These analyses were used to elucidate the seizure mechanisms of these compounds as will be discussed in more detail in the following section [9,[15][16][17][18]. In parallel, Akitane discovered new guanidine compounds: N-acetyl-c-hydroxy-L-arginine from human placenta [19], a-N-acetyl-L-arginine from cattle brain [20], a-guanidinoglutaric acid from cobalt-induced epileptogenic cerebral cortex of cats [21], and 2-guanidino ethanol in human urine [22]. Identification of the chemical structure of these new compounds is Akitane's forte.…”

Section: Neurochemical Studies On Guanidino Compoundsmentioning

confidence: 99%