Abstract
Oxidative phosphorylation and 1 α,25-dihydroxyvitamin D3 [lα,25-(OH)2D3]synthesis in isolated mitochondria were decreased by the addition of strontium. Calcium effected a similar inhibition of 1α,25-(OH)2D3 synthesis which correlated with cation-induced mitochondrial swelling. The ultrastructural changes were found to be a consequence of experimental conditions and not a prerequisite for suppressed 1α,25-(OH)2D3 synthesis. Dietary administration of strontium or calcium also resulted in a decreased rate of 1α,25-(OH)2D3 synthesis; however, the decrease in 1-hydroxylase activity was accompanied by an induction of mitochondrial 25-hydroxyvitamin D3 24-hydroxylase activity. Such an in vivo-prompted mitochondrial response occurred in the absenee of morphological changes or extensive loss of oxidative phosphorylation activity. In contrast, no induction of 24-hydroxylase activity could be observed in acute studies using isolated mitochondria. Therefore, the in vitro action of calcium and strontium does not appear to reflect the in vivo mechanism whereby the cations act to change renal 25-hydroxyvitamin D3 (25-OHD3) hydroxylation. Results from in vitro studies corcerning the action of calcium to alter renal 25-OHD3 metabolism should be interpreted in light of the cation's capacity to decrease oxidative phosphorylation and the subsequent intramitochondrial generation of NADPH.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 179-188 |
| Number of pages | 10 |
| Journal | Archives of Biochemistry and Biophysics |
| Volume | 184 |
| Issue number | 1 |
| DOIs | |
| State | Published - 1977 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Molecular Biology
Cite this
Kidney mitochondrial metabolism of 25-hydroxyvitamin D3,. Evaluation of in vitro cation modulation. / Omdahl, J. L.; Evan, Andrew.
In: Archives of Biochemistry and Biophysics, Vol. 184, No. 1, 1977, p. 179-188.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Kidney mitochondrial metabolism of 25-hydroxyvitamin D3,. Evaluation of in vitro cation modulation
AU - Omdahl, J. L.
AU - Evan, Andrew
PY - 1977
Y1 - 1977
N2 - Oxidative phosphorylation and 1 α,25-dihydroxyvitamin D3 [lα,25-(OH)2D3]synthesis in isolated mitochondria were decreased by the addition of strontium. Calcium effected a similar inhibition of 1α,25-(OH)2D3 synthesis which correlated with cation-induced mitochondrial swelling. The ultrastructural changes were found to be a consequence of experimental conditions and not a prerequisite for suppressed 1α,25-(OH)2D3 synthesis. Dietary administration of strontium or calcium also resulted in a decreased rate of 1α,25-(OH)2D3 synthesis; however, the decrease in 1-hydroxylase activity was accompanied by an induction of mitochondrial 25-hydroxyvitamin D3 24-hydroxylase activity. Such an in vivo-prompted mitochondrial response occurred in the absenee of morphological changes or extensive loss of oxidative phosphorylation activity. In contrast, no induction of 24-hydroxylase activity could be observed in acute studies using isolated mitochondria. Therefore, the in vitro action of calcium and strontium does not appear to reflect the in vivo mechanism whereby the cations act to change renal 25-hydroxyvitamin D3 (25-OHD3) hydroxylation. Results from in vitro studies corcerning the action of calcium to alter renal 25-OHD3 metabolism should be interpreted in light of the cation's capacity to decrease oxidative phosphorylation and the subsequent intramitochondrial generation of NADPH.
AB - Oxidative phosphorylation and 1 α,25-dihydroxyvitamin D3 [lα,25-(OH)2D3]synthesis in isolated mitochondria were decreased by the addition of strontium. Calcium effected a similar inhibition of 1α,25-(OH)2D3 synthesis which correlated with cation-induced mitochondrial swelling. The ultrastructural changes were found to be a consequence of experimental conditions and not a prerequisite for suppressed 1α,25-(OH)2D3 synthesis. Dietary administration of strontium or calcium also resulted in a decreased rate of 1α,25-(OH)2D3 synthesis; however, the decrease in 1-hydroxylase activity was accompanied by an induction of mitochondrial 25-hydroxyvitamin D3 24-hydroxylase activity. Such an in vivo-prompted mitochondrial response occurred in the absenee of morphological changes or extensive loss of oxidative phosphorylation activity. In contrast, no induction of 24-hydroxylase activity could be observed in acute studies using isolated mitochondria. Therefore, the in vitro action of calcium and strontium does not appear to reflect the in vivo mechanism whereby the cations act to change renal 25-hydroxyvitamin D3 (25-OHD3) hydroxylation. Results from in vitro studies corcerning the action of calcium to alter renal 25-OHD3 metabolism should be interpreted in light of the cation's capacity to decrease oxidative phosphorylation and the subsequent intramitochondrial generation of NADPH.
UR - http://www.scopus.com/inward/record.url?scp=0017708223&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0017708223&partnerID=8YFLogxK
U2 - 10.1016/0003-9861(77)90340-X
DO - 10.1016/0003-9861(77)90340-X
M3 - Article
C2 - 921291
AN - SCOPUS:0017708223
VL - 184
SP - 179
EP - 188
JO - Archives of Biochemistry and Biophysics
JF - Archives of Biochemistry and Biophysics
SN - 0003-9861
IS - 1
ER -