THE METABOLISM OF D‐α‐HYDROXY ACIDS IN ANIMAL TISSUES
THE METABOLISM OF D‐α‐HYDROXY ACIDS IN ANIMAL TISSUES
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D-α-羟基酸在动物组织中的代谢
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发表时间：
1965
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影响因子：
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通讯作者：
P. K. Tubbs
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作者：
P. K. Tubbs
到1904年（Moriya，1904），人们认识到各种动物组织形成的乳酸盐完全或几乎完全是L型。然而，几年后，Dakin和达德利（1913）发现动物组织由甲基乙二醛形成D-乳酸; Neuberg（1913）也同时发现了谷胱甘肽酶。Dakin和达德利（1913）也报道了根皮苷处理的狗从D-乳酸盐中生成葡萄糖，并提出丙酮醛是乳酸盐异构体和葡萄糖之间的中间体。其他工人（例如，Neuberg & Kobel，1929）观察到许多生物材料从己糖二磷酸形成甲基乙二醛，并且该化合物被普遍接受为糖酵解中间体。Meyerhof（1933）写道：“. .整个生物化学界都认为乳酸的形成必须以丙酮醛为中间体。”由谷胱甘肽酶形成的乳酸盐是D-型的事实似乎并没有使这些理论受挫。D-乳酸盐容易形成葡萄糖，但并非不受挑战就通过;科里和科里（1928）报告称，在禁食大鼠中，D-乳酸盐几乎不产生糖原，其利用率约为L-异构体的四分之一。超过30%的D-乳酸盐通过尿液排出，而L-异构体则没有。Meyerhof和Lohmann（1926）还发现，肝脏只容易从L-乳酸生成碳水化合物，而各种组织制备物的呼吸几乎不受D-乳酸的刺激。在1931-32年，有强有力的证据表明，丙酮醛和D-乳酸是一种重要的代谢中间体（参见Lohmann，1931 & 1932）。除其他外，还显示谷胱甘肽是谷胱甘肽酶的辅因子，而透析肌肉提取物的糖酵解需要腺苷磷酸和镁，并且不受谷胱甘肽缺乏的影响。随着这些发现，D-乳酸盐从生物化学领域消失了大约20年。在1951-53年，马勒和他的同事（Huennekens等人，1951年;马勒等人，1952年; Mahler & Huennekens，1953）报道肝和肾线粒体仅将D-乳酸氧化为丙酮酸，并且这不需要吡啶核苷酸。鸽肌颗粒呈相反的立体感。特异性;据报道，在肝和肾细胞质组分中存在一种“因子”，其被认为是乳酸消旋酶，能够使任一种线粒体氧化两种乳酸盐。D-乳酸被认为是丙酸代谢的中间体，但后来的工作并不支持这一点。虽然已经证实了上述的α 1立体特异性，但是，
By 1904 (Moriya, 1904) it was recognized that the lactate formed by various animal tissues was entirely, or almost entirely, the L-form. A few years later, however, Dakin and Dudley (1913) found that animal tissues formed D-lactate from methylglyoxal; Neuberg (1913) also discovered glyoxalase a t the same time. Dakin and Dudley (1913) also reported that phlorizin-treated dogs formed glucose from D-lactate, and proposed methylglyoxal as an intermediate between both lactate isomers and glucose. Other workers (e.g., Neuberg & Kobel, 1929) observed methylglyoxal formation from hexose diphosphate by many biological materials, and this compound became generally accepted as a glycolytic intermediate. Thus Meyerhof (1933) wrote: “. . . the whole biochemical world was seized with the idea that lactic acid formation must take place with methylglyoxal as an intermediate.” The fact that the lactate formed by glyoxalase was the D-form seems not to have discouraged these theories. That D-lactate readily formed glucose did not pass unchallenged; Cori and Cori (1928) reported that it gave rise to little glycogen in fasted rats, and was utilized a t roughly one-fourth the rate of the L-isomer. Over 30 per cent of administered D-lactate was excreted in the urine, compared with none of the L-isomer. Meyerhof and Lohmann (1926) also found that liver only formed carbohydrate readily from L-lactate, and that the respiration of various tissue preparations was barely stimulated by the D-form. In 1931-32, strong evidence was forthcoming against the idea that methylglyoxal, and hence D-lactate, was an important metabolic intermediate (see Lohmann, 1931 & 1932). I t was shown, inter alia, that glutathione was the cofactor for glyoxalase, while glycolysis by dialyzed muscle extracts required adenosine phosphates and magnesium, and was unaffected by lack of glutathione. With these findings D-lactate vanished from the biochemical scene for some 20 years. In 1951-53, Mahler and his co-workers (Huennekens et al, 1951; Mahler et al., 1952; Mahler & Huennekens, 1953) reported that liver and kidney mitochondria oxidized only D-lactate to pyruvate, and that this did not require pyridine nucleotides. Pigeon muscle particles showed opposite stereo. specificity; a “factor,” supposed to be a lactate racemase, was reported to be present in liver and kidney cytoplasmic fractions that enabled either type of mitochondria to oxidize both lactates. D-lactate was suggested as an intermediate in propionate metabolism, but later work has not supported this. While the above mitochondria1 stereospecificities have been confirmed, it is