[Kinetics of protein kinase C activities in kidney of fetal rat after intrauterine distress].
OBJECTIVE
The aim of this study is to observe the kinetic changes of protein kinase C (PKC) activities in kidney of fetal rat after intrauterine distress (IUD), and to investigate the roles of PKC in the pathogenesis of kidney impair in IUD of fetal rat.


METHODS
SD rats pregnant for 21 days were anesthetized intraabdominally, then one side of vessels of the two horns of uterus were occluded by arterial clamp to make models of intrauterine ischemia, hypoxia (IH) and reperfusion of fetal rat. The fetal rats were divided into IH group (ischemic and hypoxic for 15 min and 30 min, 16 fetal rats for each time point), reperfusion group (ischemic and hypoxic for 30 min, then reperfused for 15 min, 30 min, 45 min, 1 h and 2 h, respectively. 16 fetal rats for each time point) and false operation group (FOG) (18 fetal rats unclamped in the other uterus horn). The kidney tissue was homogenized first, then cell membrane protein and cytoplasmic protein were extracted. Improved Takai method was used to detect the changes of PKC activities of cell membrane and cytoplasma in kidney tissue of fetal rats.


RESULTS
(1) PKC activity of cell membrane started to increase after ischemia. The PKC activity of IH group was (5.66 +/- 0.88) pmol.mg(-1).min(-1); FOG was (4.30 + 0.97) pmol.mg(-1).min(-1). The PKC activity of IH group was significantly higher than that of FOG (P < 0.01). PKC activity of cell membrane increased rapidly after reperfusion, reached a peak at 30 min, and then decreased. The PKC activity was (7.26 +/- 0.76) pmol.mg(-1).min(-1) at 15 min, (9.25 +/- 0.94) pmol.mg(-1).min(-1) at 30 min, (8.34 +/- 0.89) pmol.mg(-1).min(-1) at 45 min, (6.57 +/- 0.96) pmol.mg(-1).min(-1) at 1 h, respectively. The PKC activity of reperfusion group was significantly higher than those of FOG (P < 0.01). The PKC activity of reperfusion group was (4.64 +/- 0.96) pmol.mg(-1).min(-1) at 2 h. There was no significant difference compared with that of FOG (P > 0.05). (2) The cytoplasmic PKC activity changed in a tendency opposite to that of the cell membrane PKC activity. In IH group, the PKC activity was (9.74 +/- 1.25) pmol.mg(-1).min(-1) at 15 min, (8.47 +/- 0.84) pmol.mg(-1).min(-1) at 30 min. FOG group was (10.63 +/- 1.92) pmol.mg(-1).min(-1). Reperfusion group reached the lowest PKC activity when reperfused for 30 min, (6.60 +/- 0.94) pmol.mg(-).min(-1), with a significant difference compared with that of FOG (P < 0.01). Then the PKC activity recovered to the level of FOG when reperfused for 2 h, (9.86 +/- 1.00) pmol.mg(-1).min(-1).


CONCLUSIONS
After intrauterine ischemia, hypoxia and reperfusion, PKC moves rapidly from cytoplasm to cell membrane in kidney tissue of fetal rat. PKC may be an important intracellular second messenger. It may play an important role in kidney impair in perinatal period.
Teng
Yue-e
YE
Department of Medical Oncology, First Affiliated Hospital, China Medical University, Shenyang 110001, China.
Hu
Xiao-bin
XB
Wei
Ke-lun
KL
D000818:Animals; D002462:Cell Membrane / Q000201:enzymology; D003600:Cytosol / Q000201:enzymology; D005260:Female; D005316:Fetal Distress / Q000201:enzymology*; D007668:Kidney / Q000201:enzymology*; D011247:Pregnancy; D011493:Protein Kinase C / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000201:enzymology / Q000503:physiopathology; D015398:Signal Transduction
D011493:Protein Kinase C