Increase of Methylguanidine and Guanidinoacetic Acid in the Brain of Amygdala‐Kindled Rats

Hirayasu, Yoshio; Morimoto, Kiyoshi; Otsuki, Saburo

doi:10.1111/j.1528-1157.1991.tb05531.x

Cited by 18 publications

(11 citation statements)

References 21 publications

(16 reference statements)

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“…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). Furthermore, GAA and MG levels in bilateral amygdala were shown to increase significantly in the amygdalaor hippocampal-kindled rat (15,16), an experimental model of epilepsy (17).…”

Section: Biochemistryond Molecular Biology Internationalmentioning

confidence: 65%

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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: Biochemistryond Molecular Biology Internationalmentioning

confidence: 65%

“…Previously we observed that levels of GAA and MG markedly increase in the epileptogenic focus of the brain (5,14,15,16) and furthermore we have found that high brain levels of guanidino compounds are potent endogeneous convulsants when administrated by intracisternal injection (4, …”

Section: Discussionmentioning

confidence: 99%

Guanidino compounds generate reactive oxygen species

et al. 1996

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“…The level of MG extremely increases under the pathophysiological condition such as convulsion or chronic renal failure. For example, the levels of MG increased in the epileptogenic focus of the rat brain as experimental animals for epilepsy, i.e., the level of MG in amygdala showed significant increase in the epileptic animal models; amygdala-kindled rats [11,12]. The level of MG in the plasma increased several-fold under the uremic condition [3] when compared to the control.…”

Section: Discussionmentioning

confidence: 95%

“…In this study, it was found that ascorbate, GSH, EPC-K 1 , and Trolox, which are closely linked to redox-system in biological system, effectively inhibited •OH generation from MG, indicating the potential for the protection against the extremely high level of MG and also the prevention of MG formation [11,12,[18][19][20].…”

Section: Discussionmentioning

confidence: 99%

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Inhibitory Effect of Antioxidants on Hydroxyl Radical Generation from Methylguanidine: An ESR Study

Noda

Mankura

2008

Neurochem Res

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Methylguanidine (MG) is known as not only a nephrotoxin but also as a neurotoxine. We have previously showed that MG itself generates hydroxyl radicals (*OH) in an in vitro study. In this study, we examined the inhibitory effects of ascorbate, EPC-K(1) (alpha-tocopheryl-L-ascorbate-2-O-phosphate diester), Trolox (water-soluble vitamin E analogue), and glutathione (GSH) on *OH generation from MG using an electron spin resonance (ESR) spectrometry with spin trap 5,5-dimethyl-1-pyrroline-N-oxide (DMPO). It was found that these compounds have potent inhibitory effect on *OH generation from MG in the order of ascorbate > GSH > EPC-K(1) > Trolox.

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