An Intracellular Laccase Is Responsible for Epicatechin-Mediated Anthocyanin Degradation in Litchi Fruit Pericarp.

In contrast to the detailed molecular knowledge available on anthocyanin synthesis, little is known about its catabolism in plants. Litchi (Litchi chinensis) fruit lose their attractive red color soon after harvest. The mechanism leading to quick degradation of anthocyanins in the pericarp is not well understood. An anthocyanin degradation enzyme (ADE) was purified to homogeneity by sequential column chromatography, using partially purified anthocyanins from litchi pericarp as a substrate. The purified ADE, of 116 kD by urea SDS-PAGE, was identified as a laccase (ADE/LAC). The full-length complementary DNA encoding ADE/LAC was obtained, and a polyclonal antibody raised against a deduced peptide of the gene recognized the ADE protein. The anthocyanin degradation function of the gene was confirmed by its transient expression in tobacco (Nicotiana benthamiana) leaves. The highest ADE/LAC transcript abundance was in the pericarp in comparison with other tissues, and was about 1,000-fold higher than the polyphenol oxidase gene in the pericarp. Epicatechin was found to be the favorable substrate for the ADE/LAC. The dependence of anthocyanin degradation by the enzyme on the presence of epicatechin suggests an ADE/LAC epicatechin-coupled oxidation model. This model was supported by a dramatic decrease in epicatechin content in the pericarp parallel to anthocyanin degradation. Immunogold labeling transmission electron microscopy suggested that ADE/LAC is located mainly in the vacuole, with essential phenolic substances. ADE/LAC vacuolar localization, high expression levels in the pericarp, and high epicatechin-dependent anthocyanin degradation support its central role in pigment breakdown during pericarp browning.

[Therapeutic efficacy of bipolar plasmakinetic technique compared with transurethral resection on benign prostate hyperplasia].

OBJECTIVE: To evaluate the effect and safety of transurethral prostatectomy with the bipolar plasmakinetic technique (PKRP) compared with the transurethral resection (TURP) in the treatment of benign prostate hyperplasia (BPH). METHOD: Four hundred BPH patients with matched lesions were divided into 2 groups: 200 patients, aged 74.1 (58-91), underwent transurethral prostatectomy with PKRP, and 200 patients, aged 73.8 (56-90), underwent TURP. RESULT: In the PKRP group the average IPSS decreased from 27.1 +/- 4.5 preoperatively to 11.3 +/- 3.4 postoperatively 6 months after (P < 0.01), the. average maximum flow-rate Q (max) increased from 6.1 +/- 2.4 ml/s preoperatively to 18.6 +/- 3.5 ml/s postoperatively (P < 0.01), and the average residual urine (RU) reduced from 102.3 +/- 43.3 ml preoperatively to 22.6 +/- 16.3 ml after the operation (P < 0.01). However in the TURP group the average IPSS decreased from 26.9 +/- 4.2 preoperatively to 10.8 +/- 3.6 6 months after the operation (P < 0.01), the Q (max) increased from 5.7 +/- 2.4 ml/s preoperatively to 19.1 +/- 3.7 ml/s postoperatively (P < 0.01), and the average RU decreased from 102.3 +/- 43.3 ml preoperatively to 22.6 +/- 16.3 ml after the operation (P < 0.01). There were no significant differences in these parameters between these 2 groups (all P > 0.05). The average catheter retention time was 31.5 h in the PKRP, significantly shorter than that in the TURP group (61.5 hours, P < 0.01). The incidence rate of post-operational asynodia in the PKRP group was 14.3%, not significantly different from that in the TURP group (15.2%, P > 0.05). During the operation no hemorrhage or transurethral resection syndrome (TURS) occurred in the PKRP group, however, there were 5 cases of TURS and 18 cases of blood transfusion in the TURP group. CONCLUSION: PKRP has the same therapeutic efficacy as TURP on BPH. Moreover, it was more cheaper and with lower complication than TURP.