Journal of Health Science
Online ISSN : 1347-5207
Print ISSN : 1344-9702
ISSN-L : 1344-9702
REGULAR ARTICLES
Hyperosmolarity Induced Cystine Transport and Cystine-cysteine Cycle between Erythrocytes and the Plasma
Deniz YildizYeliz Çakir
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2008 Volume 54 Issue 2 Pages 187-195

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Abstract

The objective of the present study was to determine if a cystine-cysteine cycle operates between the erythrocytes and the plasma. In the present study we incubated the erythrocytes in krebs ringer phosphate buffer with different osmolarity containing different amounts of cystine. Our results show that erythrocytes do not uptake cystine from the environment when the osmolarity of the buffer is 310 mOsmol/l. Erythrocytes also do not operate a cystine-cysteine cycle in this isoosmolar buffer. However, when exposed to hyperosmolar buffer in the ranges that occur in the kidney medulla which is in between 1200-1400 mOsmol/l erythrocytes start to uptake cystine from the environment and induce a cystine-cysteine cycle. The cystine uptake and cystine-cysteine cycle were characterized by measurement of changes in the free -SH concentrations in erythrocytes and in the buffer. Following incubation of erythrocytes in 1 mM cystine containing 1250 and 1300 mOsmol/l buffer, the free -SH concentrations in the buffer reached to 0.102±0.002 and 0.241±0.013 μmol/ml erythrocyte respectively. Our results demonstrate that erythrocytes display a cystine-cysteine cycle in hyperosmolar environment which is prevailed mainly in the kidney medulla. Our results also display that this process is biologically active and energy dependent. The observed cystine-cysteine cycle is inhibited when the erythrocytes are incubated at lower temperatures and in the absence of glucose. Our results suggest that erythrocytes uptake cystine, intracellulary reduce it to cysteine and release it back to the environment when exposed to hyperosmolar conditions. Erythrocytes may have a role in the regulation of plasma cystine and cysteine concentrations and may contribute to the regulation of plasma redox status.

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© 2008 by The Pharmaceutical Society of Japan
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