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肝切除大鼠中由[14C1]乙醇酸和[14C1]乙醛酸合成草酸盐的过程。

Oxalate synthesis from [14C1]glycollate and [14C1]glyoxylate in the hepatectomized rat.

作者信息

Farinelli M P, Richardson K E

出版信息

Biochim Biophys Acta. 1983 May 4;757(1):8-14. doi: 10.1016/0304-4165(83)90146-0.

DOI:10.1016/0304-4165(83)90146-0
PMID:6838909
Abstract

Hepatectomy significantly altered the metabolism of [1-14C]glyoxylate and [1-14C]glycollate in the rat. The production of 14CO2 was reduced by 47% and 77-86%, respectively, indicating the involvement of the liver in the oxidation of both substrates. Unidentified intermediates, assumed to be primarily glycine, serine and ethanolamine, were also reduced by over 50%, as would be expected from the removal of the aminotransferase enzymes through the hepatectomy. The biosynthesis of [14C]oxalate from [1-14C]glycollate was reduced by more than 80% in the hepatectomized rat. This suggests that this oxidation is primarily catalyzed by the liver enzymes, glycolic acid oxidase and glycolic acid dehydrogenase, in the intact rat. The limited formation of [14C]oxalate from [14C1]glycollate observed in the hepatectomized rat is probably catalyzed by lactate dehydrogenase or extrahepatic glycolic acid oxidase. Hepatectomy did not significantly alter the rate of formation of [14C]oxalate from [14C1]glyoxylate. However, since saturating concentrations of glyoxylate could not be used because of the toxicity of this substrate, the involvement of glycollic acid oxidase in this oxidation reaction in the intact rat can not be ruled out. In the hepatectomized rat, lactate dehydrogenase appears to be the enzyme making the major contribution, although other as yet not identified enzymes may be contributing. The increased deposition of oxalate in the tissues, oxalosis, may result from the shift in oxalate synthesis from the liver to the extrahepatic tissues.

摘要

肝切除术显著改变了大鼠体内[1-¹⁴C]乙醛酸和[1-¹⁴C]乙醇酸的代谢。¹⁴CO₂的生成分别减少了47%和77 - 86%,这表明肝脏参与了这两种底物的氧化过程。假定主要为甘氨酸、丝氨酸和乙醇胺的未鉴定中间产物也减少了50%以上,这与肝切除术后转氨酶的去除所预期的情况相符。在肝切除大鼠中,由[1-¹⁴C]乙醇酸生成[¹⁴C]草酸盐的生物合成减少了80%以上。这表明在完整大鼠中,这种氧化主要由肝脏酶——乙醇酸氧化酶和乙醇酸脱氢酶催化。在肝切除大鼠中观察到的由[¹⁴C]乙醇酸生成[¹⁴C]草酸盐的有限生成可能由乳酸脱氢酶或肝外乙醇酸氧化酶催化。肝切除术并未显著改变由[¹⁴C]乙醛酸生成[¹⁴C]草酸盐的速率。然而,由于该底物具有毒性而无法使用饱和浓度,因此不能排除完整大鼠中乙醇酸氧化酶参与此氧化反应的可能性。在肝切除大鼠中,乳酸脱氢酶似乎是起主要作用的酶,尽管可能还有其他尚未鉴定的酶也在发挥作用。草酸盐在组织中的沉积增加,即草酸中毒,可能是由于草酸盐合成从肝脏转移到了肝外组织所致。

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