Abstract
Methylguanidine (MG) is known to accumulate in body fluids of uremic and hemodialysis patients1–2 and has been proved to be a strong uremic toxin3. It was reported that erythrocyte deformability and Na+,K+— ATPase activity of erythrocyte membranes decreased in hemodialysis patients and there was a significant negative correlation between erythrocyte deformability and MG level4. Recent reports reveal that MG is converted from creatinine (CRN) by the action of various species of active oxygen, especially hydroxyl radicals as produced in the Fenton reaction5–6 and that free hemoglobin acts as a biological Fenton reagent to generate hydroxyl radicals7, and as an iron promoter in the Fenton reaction8. Since free radicals were shown to play an unfavorable role renal failure9–11, determination of MG in body fluids as a marker for hydroxyl radicals could prove useful in clinical practice.
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References
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© 1989 Plenum Press, New York
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Nakajima, Mo., Nakamura, K., Shirokane, Y., Hirasawa, Y. (1989). Enzymic Determination of Methylguanidine in Serum and Plasma of Hemodialysis Patients as a Marker for Hydroxyl Radicals. In: Mori, A., Cohen, B.D., Koide, H. (eds) Guanidines 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0821-8_1
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DOI: https://doi.org/10.1007/978-1-4613-0821-8_1
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