Kakuma S, Leevy C B, Frank O, Baker H
Vitamin Laboratories, New Jersey Medical School, Newark 07107.
Alcohol Alcohol. 1989;24(1):31-4.
Methods were evaluated for depressing the acetaldehyde (AcH) inhibition of uridine uptake by Chang liver cells and isolated autologous liver cells, obtained by percutaneous liver biopsy from cases of alcoholic hepatitis. Hepatocytes so obtained were significantly more susceptible to AcH-induced inhibition of uridine uptake than hepatocytes from normal liver, alcoholic fatty liver, stable alcoholic cirrhosis and acute viral hepatitis. Benzylamine (an aldehyde buffer) and pyridoxal-5' phosphate (PLP) counteracted the inhibition of uridine uptake by AcH in vitro. We suggest that benzylamine neutralizes AcH toxicity through a Schiff-base condensation with AcH thus taking AcH out of the field of action. PLP protects against AcH-induced inhibition of uridine uptake by probably forming a Schiff base with cellular amino acids thus blocking further condensation of these amino groups with AcH. In this manner, uridine uptake by liver cells for RNA synthesis can proceed without interference by AcH.
对通过经皮肝穿刺活检从酒精性肝炎患者获取的Chang肝细胞和分离的自体肝细胞，评估了降低乙醛（AcH）对尿苷摄取抑制作用的方法。如此获得的肝细胞比来自正常肝脏、酒精性脂肪肝、稳定期酒精性肝硬化和急性病毒性肝炎的肝细胞对AcH诱导的尿苷摄取抑制作用更敏感。苄胺（一种醛缓冲剂）和磷酸吡哆醛（PLP）在体外可对抗AcH对尿苷摄取的抑制作用。我们认为苄胺通过与AcH形成席夫碱缩合来中和AcH毒性，从而使AcH脱离作用范围。PLP可能通过与细胞氨基酸形成席夫碱来防止AcH诱导的尿苷摄取抑制，从而阻止这些氨基与AcH的进一步缩合。通过这种方式，肝细胞用于RNA合成的尿苷摄取可以不受AcH干扰地进行。
