Konjević Gordana, Jurisić V, Jakovljević B, Spuzić I
Glas Srp Akad Nauka Med. 2002(47):137-47.
Serum LDH level is a prognostic factor in different malignancies as its increase reflects tumor mass and response to therapy. Serum LDH is the consequence of the disruption of the cell membrane of a large fraction of dividing malignant cells whose metabolic hallmark is anaerobic glycolysis that leads to increased LDH enzyme activity. Moreover, as we have previously shown that spontaneous LDH release from cells represents a measure of cell membrane damage, and this parameter is used for the estimation of cell destruction in cytotoxic assays, the aim of this study was to evaluate the characteristics of LDH activity of PBMC of patients with different solid tumors (non-Hodgkin's lymphomas--NHL, n=47; Hodgkin's disease--HD, n=45; ovarian cancer--OvCa, n=6; breast cancer--BrCa, n=34; thyroid cancer--TyCa, n=3; cancer of PVU--CaPVU, n=4 and head & neck--H&N, n=6) in all clinical stages of NHL and HD and in advanced clinical stages of disease for BrCa, OvCa, CaPVU and H&N. Spontaneous LDH release from PBMC was determined by the spectrophotometric method from supernatants of 8 x 10(6)/ml PBMC cultured for 2 h in RPMI 1640 without phenol red using and LDH substrate mixture. The total LDH activity was determined after lysis of PBMC by ultrasound. The obtained results indicate that PBMC in all the investigated malignancies, compared to control PBMC, demonstrate a significant increase (p<0.01) in spontaneous LDH release act, which correlates with advanced clinical stage in all malignancies except in Hodgkin's disease, in which the spontaneous LDH release was increased in all clinical stages. Contrary to this, the total LDH activity was not increased in PBMC in all investigated tumors. However, the "percent of spontaneous LDH release" was always increased, regardless of the total LDH activity, indicating that spontaneous LDH release is the consequence of PBMC membrane damage present in advanced stages of different solid tumors.
血清乳酸脱氢酶（LDH）水平是不同恶性肿瘤的一个预后因素，因为其升高反映了肿瘤大小及对治疗的反应。血清LDH是大部分正在分裂的恶性细胞细胞膜破坏的结果，这些细胞的代谢特征是无氧糖酵解，会导致LDH酶活性增加。此外，正如我们之前所表明的，细胞自发释放LDH代表细胞膜损伤程度，该参数用于细胞毒性试验中细胞破坏的评估。本研究的目的是评估不同实体瘤患者（非霍奇金淋巴瘤——NHL，n = 47；霍奇金病——HD，n = 45；卵巢癌——OvCa，n = 6；乳腺癌——BrCa，n = 34；甲状腺癌——TyCa，n = 3；肾盂输尿管癌——CaPVU，n = 4；头颈部癌——H&N，n = 6）外周血单个核细胞（PBMC）的LDH活性特征，这些患者涵盖NHL和HD的所有临床分期以及BrCa、OvCa、CaPVU和H&N的疾病晚期。采用分光光度法，从在不含酚红的RPMI 1640培养基中培养2小时的8×10⁶/ml PBMC上清液中，使用LDH底物混合物测定PBMC的自发LDH释放量。通过超声裂解PBMC后测定总LDH活性。所得结果表明，与对照PBMC相比，所有研究的恶性肿瘤患者的PBMC自发LDH释放活性均显著增加（p<0.01），除霍奇金病外，这与所有恶性肿瘤的晚期临床分期相关，霍奇金病在所有临床分期中自发LDH释放均增加。与此相反，所有研究肿瘤患者的PBMC总LDH活性并未增加。然而，无论总LDH活性如何，“自发LDH释放百分比”总是增加的，这表明自发LDH释放是不同实体瘤晚期PBMC膜损伤的结果。
