Shennan D B, Thomson J
Hannah Research Institute, Ayr KA6 5HL, Scotland, UK.
Mol Cell Biochem. 2004 Jul;262(1-2):111-8. doi: 10.1023/b:mcbi.0000038223.21650.5e.
A knowledge of volume-sensitive solute transport in mammary cells is important in light of evidence that mammary cell metabolism is regulated by the cellular hydration state. In this report we have examined volume-sensitive taurine and K+ (Rb+) transport by lactating rat mammary tissue. A hyposmotic shock increased taurine efflux from rat mammary tissue: taurine release returned to a basal level upon transferring the tissue back to an isosmotic medium. However, the time taken to activate taurine efflux was less than the time taken to inactivate taurine release. A second subsequent osmotic challenge also increased taurine release but to a lesser extent than the first osmotic shock. A similar pattern was observed for bumetanide-insensitive, volume-activated K+ (Rb+) release from mammary tissue explants suggesting that taurine and K+ efflux are acting in concert to regulate mammary cell volume. An abrupt hyposmotic shock increased taurine efflux from mammary explants to a greater extent than a gradual reduction in the osmolality of the incubation medium. Increasing extracellular K+ increased taurine release via a pathway sensitive to niflumic acid, which suggests that activation of volume-sensitive taurine efflux does not require a change in the ionic strength of the incubation medium or a decrease in intracellular osmolality. A hyposmotic shock also stimulated taurine efflux from rat mammary acini. In contrast, a hyposmotic challenge had no effect on taurine uptake measured under sodium-free conditions. Hyposmotically induced taurine efflux was not dependent upon extracellular calcium. The results suggest that taurine and K+ transport may allow mammary cells to volume-regulate and consequently help to control mammary metabolism.
鉴于有证据表明乳腺细胞代谢受细胞水合状态调节,了解乳腺细胞中对容积敏感的溶质转运非常重要。在本报告中,我们研究了泌乳大鼠乳腺组织对容积敏感的牛磺酸和钾离子(铷离子)转运。低渗休克增加了大鼠乳腺组织中牛磺酸的外流:将组织转回等渗培养基后,牛磺酸释放恢复到基础水平。然而,激活牛磺酸外流所需的时间比使牛磺酸释放失活所需的时间短。随后的第二次渗透挑战也增加了牛磺酸的释放,但程度小于第一次渗透休克。从乳腺组织外植体中观察到对布美他尼不敏感、容积激活的钾离子(铷离子)释放也有类似模式,这表明牛磺酸和钾离子外流共同作用以调节乳腺细胞容积。突然的低渗休克比孵育培养基渗透压的逐渐降低更能增加乳腺外植体中牛磺酸的外流。增加细胞外钾离子通过对氟尼酸敏感的途径增加牛磺酸释放,这表明激活对容积敏感的牛磺酸外流不需要孵育培养基离子强度的改变或细胞内渗透压的降低。低渗休克也刺激了大鼠乳腺腺泡中牛磺酸的外流。相比之下,低渗挑战对在无钠条件下测量的牛磺酸摄取没有影响。低渗诱导的牛磺酸外流不依赖于细胞外钙。结果表明,牛磺酸和钾离子转运可能使乳腺细胞进行容积调节,从而有助于控制乳腺代谢。