The overall cellular gene expression is well realized by the coordinated regulation between nuclear DNA and mitochondria DNA. Coordinated regulation between two genomes plays a key role not only in mitochondria biogenesis and protein synthesis but also more importantly in the regulation of gene expression of mitochondria respiratory chain subunits in order to mediate the mitochondrial respiratory function. In the present review, we focus on the mechanism of coordinated regulation between two genomes.

The inhibitory effects of actinomycin D on chromatin (or DNA) template and the stimulating effects of synthetic template Poly [d(A-T)] on transcription were observed in the liver nucleic transcriptional system of the rat in vitor.By introducing proper concentrations of actinomycin D and Poly [d(A-T)] into each reactionary system,a method to assay free RNA polymerase activity in the nucleus was established.In addition,a comparison of the contents between chromatin-engaged and free polymerase in normal rat liver nuclei isolated with hypertonic sucrose (2.3 mol/L) was made.Eventually,the possible role free RNA Polymerases play in the eukaryotic transcriptional process was discussed.

Classroom teaching is the focus of teaching of school and main approach to medicine course,and the quality of classroom teaching is directly related to the development of students.Thus improving classroom teaching is very important to increase integral teaching of school.This paper discusses how to increase the thinking ability of students in classroom teaching.

We have reformed the traditional pathophysiological experimental teaching from improving experimental teaching method,optimizing experimental content,updating experimental teaching material,starting design experimental and founding general examine system.

Aim To understand the changing aspects of CAP-administration on expression of cytochrome C oxidase(COX) subunits I and IV and their mechanisms regulated by gene expression encoded by mtDNA and nDNA. Methods Wistar rats were randomly divided into control and CAP groups, Rats were administrated CAP(100 mg?kg -1, intraperitoneal injection) every 12 hours for 7 days before sacrificed by decapitation. Rat brain was removed and the cerebral cortex mitochondria was isolated by centrifugation programme. The protein content of COX subunitⅠand Ⅳ in mitochondria and NRF-1 in cerebral tissues was detected by Western blot analysis. And mRNA state levels of COXⅠ, COXⅣ, mtTFA and NRF-1 in tissues were determined by RT-PCR.Results Compared with C group, a decreased protein content of COX subunitⅠand an elevated ratio of subunit Ⅳ/Ⅰwas observed in CAP group, The protein content of COX subunit Ⅳ and NRF-1 as well as COXⅠ,Ⅳ,NRF-1 and mtTFA mRNA state level was not unchanged between the two groups. Conclusion The change of content of COX subunitⅠprotein in mitochondria from cerebral cortex showed there is no regulation of feedback to mitochondrial and nuclear transcription. The nuclear genomes expression does not correspond to mitochondrial expression in CAP-administrated rats.

Objective To understand the changing aspects of CAP-administration on mitochondrial oxidative phosphorylation function and cytochrome c oxidase (COX) activity during hypoxia exposure and their mechanisms. Methods Except the control group (C group), adult male Wistar rats were exposed to a hypobaric chamber simulated 5 000-meter high altitude for 23 h every day for 0, 1, 5, 15, 30 d (H_ 0, 1, 5, 15, 30 ) respectively and administrated CAP (100 mg/kg, intraperitoneal injection) every 12 h for 7 d before sacrificed by decapitation. Mitochondrial respiratory function and COX activity were measured by Clark oxygen electrode and polarography, respectively. Results As compared with C group, mitochondrial state 3 respiration (ST_3) and respiratory control rate (RCR) and oxidative phosphorylation rate (ORP) and COX activity in H_0+CAP group all decreased significantly, but by prolonging hypoxia exposure increased and restored to the control level. Conclusion Mitochondrial respiratory function, oxidative phosphorylation efficiency and COX activity in rat brain could improve by administrating CAP during hypoxia exposure and almost reach to the control level by prolonging hypoxia exposure.

Objective To observe the changes of rat brain mitochondrial uncoupling protein (UCP) content and activity, and explore the effect of UCP on mitochondrial energy metabolism during hypoxia exposure. Methods Adult SD rats were set randomly into control and hypoxia group (n=8 in each group). The rats of hypoxia group were put into a hypobaric chamber simulating 5000-meter high altitude for 3 days (23 h/d). The brain mitochondria was isolated by centrifugation. Mitochondrial oxidative respiratory function was measured by Clark oxygen electrode. Mitochondrial membrane potential was detected by Rhodamine123 method. The content of adenine nucleotide pool (ATP, ADP, AMP) in mitochondria was measured by high performance liquid chromatography. UCP content and activity were detected by [~ 3 H]-GTP binding method. Results High altitude hypoxia resulted in significant increase of UCP activity and a 2.9-fold rise of UCP content of rats (P

Objective To investigate effect of guanosine diphosphate (GDP) on the mitochondrial respiratory oxygen consumption and the mitochondrial membrane potential (MMP) of rat brain and explore the relationship of the change of uncoupling proteins (UCPS) activity with the oxygen consumption and MMP. Methods The mitochondria of rat brain were isolated by centrifugation. Mitochondria oxidative respiratory consumption was measured by Clark electrode after the treatment of GDP at different concentrations so as to calculate mitochondrial state 3 respiration (ST3), mitochondrial state 4 respiration (ST4), respiratory control rate (RCR), and the rate of oxidative phosphorylation (OPR). MMP was detected by Rhodamine 123 method at the different concentrations of GDP. Results With the increase of GDP concentration form 0 to 1.0 mmol/L, the values of ST3, ST4 and OPR were reduced while RCR was elevated. But when the concentration increased to 1.4 mmol/L, the former 3 indexes begun to increase while the later declined. When the GDP concentration reached to 1 mmol/L, the inhibitory rate was only 35.1%, 51.3%, 14.2% to ST3, ST4 and OPR respectively, while RCR was increased to 133.2%. No matter the concentration was over 1 mmol/L or under 1 mmol/L, the ability of inhibition was attenuated. MMP reached to the highest point when GDP exerted the highest inhibitory rate on mitochondrial respiratory oxygen consumption. Conclusion GDP, an inhibitor of UCPS, can regulate the respiratory oxygen consumption and MMP of the isolated rat brain mitochondrial directly in a dose-effect fashion. The change of UCPS activity can affect the respiratory oxygen consumption and MMP.

AIM: To explore the changes of myocardial energy metabolism and adenine nucleotide translocase (ANT) activity in mitochondria in rats exposed to hypoxia. METHODS: Adult male Wistar rats were exposed to simulated high altitude at 5 000 m for control (0 d), 1 d, 5 d, 15 d, 30 d in hypobaric chamber. Myocardial mitochondria were isolated by centrifugation. Mitochondria respiratory function was measured by Clark oxygen electrode. The size of adenine nucleotides pool (ATP, ADP, AMP) in mitochondria were separated and measured by HPLC. ANT activity was measured by [3H]-ADP incorporation. RESULTS: Compared to control, mitochondria state Ⅲ respiratory (ST_3) and RCR decreased and ST_4 increased sharply at 1 d, 5 d and 15 d, ST_3 still lower than that in control at 30 d, while RCR level restored. ATP contents and ANT activity decreased at 1 d and 5 d, then restored to control level at 15 d, then decreased again at 30 d. CONCLUSION: The inhibition of mitochondria respiratory function is the main reason that makes ATP contents decrease during hypoxic exposure. ANT activity and ATP content change cooperatively.

AIM:To observe the effect of GDP on uncoupling proteins(UCPs) activity and the efficiency of oxidative phosphorylation in hypoxic exposed rat brain mitochondria.METHODS: Adult SD rats were randomly divided into three groups (control, acute hypoxia and chronic hypoxia groups). The animals were placed into a hypobaric chamber simulated 5 000 m high altitude for 0, 3 and 30 d, respectively. The mitochondria from rat brain were isolated by centrifugation. The activity of UCPs was detected by the method of [H3]-GTP binding with UCPs specifically. The maximal binding content (Bmax) and the dissociation constant (Kd) were determined by Scatchard plot. The mitochondrial potential was measured by rhodamine 123 method. Oxidative respiratory consumption was measured by Clark electrode. The experiments were conducted under the conditions with or without GDP (1 mmol/L), respectively. RESULTS: For exposed to hypoxia, Bmax and the oxidative consumption of uncoupling respiration were increased. Kd, MMP and RCR were decreased. UCPs activity was inhibited by GDP in three groups. Kd was increased 61.01%, 83.13% and 71.52% and Bmax was decreased 23.18%, 35.20% and 33.38%, respectively. The values in the acute hypoxic group were changed markedly. The sensitivity of UCPs to GDP was elevated significantly by hypoxia. With the reducing of UCPs activity, oxidative consumption of uncoupling respiration was decreased whereas RCR and MMP were increased. The results elucidated increase in the efficiency of oxidative phosphorylation.CONCLUSION: GDP increases the mitochondrial membrane potential and decreases the oxygen consumption of uncoupling respiration in hypoxic exposed rat brain mitochondria by inhibiting UCPs activity. The results suggest that the change in UCPs activity is one of the factors of mitochondrial dysfunction in oxidative phosphorylation induced by hypoxia.