Published online Jul 28, 2014. doi: 10.3748/wjg.v20.i28.9585
Revised: March 26, 2014
Accepted: April 21, 2014
Published online: July 28, 2014
Processing time: 166 Days and 21.4 Hours
AIM: To determine the alterations in rat enterocyte mitochondrial respiratory function and enzyme activities following traumatic brain injury (TBI).
METHODS: Fifty-six male SD rats were randomly divided into seven groups (8 rats in each group): a control group (rats with sham operation) and traumatic brain injury groups at 6, 12, 24 h, days 2, 3, and 7 after operation. TBI models were induced by Feendy’s free-falling method. Mitochondrial respiratory function (respiratory control ratio and ADP/O ratio) was measured with a Clark oxygen electrode. The activities of respiratory chain complex I-IV and related enzymes were determined by spectrophotometry.
RESULTS: Compared with the control group, the mitochondrial respiratory control ratio (RCR) declined at 6 h and remained at a low level until day 7 after TBI (control, 5.42 ± 0.46; 6 h, 5.20 ± 0.18; 12 h, 4.55 ± 0.35; 24 h, 3.75 ± 0.22; 2 d, 4.12 ± 0.53; 3 d, 3.45 ± 0.41; 7 d, 5.23 ± 0.24, P < 0.01). The value of phosphate-to-oxygen (P/O) significantly decreased at 12, 24 h, day 2 and day 3, respectively (12 h, 3.30 ± 0.10; 24 h, 2.61 ± 0.21; 2 d, 2.95 ± 0.18; 3 d, 2.76 ± 0.09, P < 0.01) compared with the control group (3.46 ± 0.12). Two troughs of mitochondrial respiratory function were seen at 24 h and day 3 after TBI. The activities of mitochondrial complex I (6 h: 110 ± 10, 12 h: 115 ± 12, 24 h: 85 ± 9, day 2: 80 ± 15, day 3: 65 ± 16, P < 0.01) and complex II (6 h: 105 ± 8, 12 h: 110 ± 92, 24 h: 80 ± 10, day 2: 76 ± 8, day 3: 68 ± 12, P < 0.01) were increased at 6 h and 12 h following TBI, and then significantly decreased at 24 h, day 2 and day 3, respectively. However, there were no differences in complex I and II activities between the control and TBI groups. Furthermore, pyruvate dehydrogenase (PDH) activity was significantly decreased at 6 h and continued up to 7 d after TBI compared with the control group (6 h: 90 ± 8, 12 h: 85 ± 10, 24 h: 65 ± 12, day 2: 60 ± 9, day 3: 55 ± 6, day 7: 88 ± 11, P < 0.01). The changes in α-ketoglutaric dehydrogenase (KGDH) activity were similar to PDH, except that the decrease in KGDH activity began at 12 h after TBI (12 h: 90 ± 12, 24 h: 80 ± 9, day 2: 76 ± 15, day 3: 68 ± 7, day 7: 90 ± 13, P < 0.01). No significant change in malate dehydrogenase (MDH) activity was observed.
CONCLUSION: Rat enterocyte mitochondrial respiratory function and enzyme activities are inhibited following TBI. Mitochondrial dysfunction may play an important role in TBI-induced gastrointestinal dysfunction.
Core tip: Many researchers over the years have attempted to reveal the possible mechanism involved in gastrointestinal dysfunction following traumatic brain injury (TBI). Mitochondria are thought to be the primary target of oxidative damage and play an important role in oxidative stress. However, alterations in rat enterocyte mitochondrial respiratory function and enzyme activities following TBI have not been described previously. The purpose of this study was to determine the effect of TBI on rat enterocyte mitochondrial respiratory function and enzyme activities, as well as to reveal the alterations in rat enterocyte mitochondrial function following TBI.