Effect of various ambient temperatures on activities of mitochondrial complex II in patients of deficiency-cold syndrome and deficiency-heat syndrome / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To explore activity laws of mitochondrial complex II in patients of deficiency-cold syndrome (DCS) and deficiency-heat syndrome (DHS) under various ambient temperatures.</p><p><b>METHODS</b>Subjects were recruited by questionnaire and expert diagnosis from grade 1 - 3 undergraduates at Henan College of Traditional Chinese Medicine in November 2012, and assigned to a normal control group, the DCS group, and the DHS group, 20 in each group. Their venous blood samples were collected at two different temperature conditions. Activities of mitochondrial complex II were measured by spectrophotometry.</p><p><b>RESULTS</b>(1) Comparison of mitochondrial complex It under various ambient temperatures: Compared with room temperature in the same group, activity values were all increased in the normal control group at cold temperature with significant difference (P <0.05), but there was no significant difference in the DCS group and the DHS group (P >0. 05). Compared with the normal control group, activity values of complex H were reduced in the DCS group at cold and room temperatures with significant difference (P <0.05). Compared with the DCS group, activity values of complex It were increased in the DHS group with significant difference (P <0. 05). (2) Changes of adjustment rates: Compared with room temperature, the adjustment rate all rose at cold temperature in the normal control group and the DHS group with significant difference (P <0.05), but with no significant difference found in the DCS group (P >0. 05). Compared with the normal control group at the same temperature, the adjustment rate in the DHS group and the DCS group was all reduced at cold and room temperatures with significant difference (P <0. 05). There were no significant difference in the adjustment rate between the DHS group and the DCS group (P > 0. 05).</p><p><b>CONCLUSIONS</b>Environment temperature can affect the activity of mitochondrial complex II with different influence degrees on different syndrome types of people, but its change trend are basically identical.</p>

Fiebre chikungunya en México: caso confirmado y apuntes para la respuesta epidemiológica / Chikungunya fever in Mexico: confirmed case and notes on the epidemiologic response

La fiebre chikungunya (CHIK) es una enfermedad viral transmitida al ser humano por el mismo vector del dengue, el mosquito Aedes. Además de fiebre y fuertes dolores articulares, produce otros síntomas como mialgias, cefalea, náuseas, cansancio y exantema. No tiene tratamiento específico; el manejo terapéutico de los pacientes se enfoca en el alivio de los síntomas. Históricamente se han reportado brotes de grandes proporciones; incluso desde 2010 se llegó a considerar como una potencial epidemia emergente. En 2013 se introdujo a las islas del Caribe y recientemente se ha reportado en el continente americano. En este trabajo se describe el primer caso confirmado de chikungunya en México, en el municipio de Tlajomulco de Zúñiga, Jalisco, en mayo de 2014, importado de la isla Antigua y Barbuda, en el Caribe, por una mujer de 39 años de edad.

Chikungunya fever (CHIK) is a viral disease transmitted to human beings by the same vector as dengue -the Aedes mosquito. Besides fever and severe pain in the joints, it produces other symptoms such as myalgias, headache, nausea, fatigue and exanthema. There is no specific treatment for it; the therapeutic management of patients focuses on symptom relief. Historically, outbreaks of large proportions have been reported; even since 2010 it was considered to be a potential emerging epidemic. In 2013 it was introduced into the islands of the Caribbean, and it has recently been reported in the American continent. This paper describes the first confirmed case of chikungunya in Mexico -in the municipality of Tlajomulco de Zúñiga, Jalisco, in May, 2014-, which was imported from the Caribbean island of Antigua and Barbuda by a 39 year-old woman.

Mitochondrial respiratory chain complex Ⅱ deficiency and diseases / 中国当代儿科杂志

This article reviews the structure and function of mitochondrial respiratory chain complex Ⅱ, and the clinical features, diagnosis, treatment and genetic analysis of mitochondrial respiratory chain complex Ⅱ deficiency. Mitochondrial complex Ⅱ, known as succinate dehydrogenase, is a part of the mitochondrial respiratory chain. It plays an important role in cellular oxidative phosphorylation. It is associated with oxidative stress and is a sensitive target for toxic substances and abnormal metabolin in cells. Clinical manifestations of respiratory chain complex Ⅱ deficiency are characterized by a wide variety of abnormalities. Progressive neuromuscular dysfunction is the most common syndrome. Cardiomyopathy, episodic vomit and hemolytic uremic syndrome are also encountered in a few cases. A precise diagnosis is dependent on enzyme activities assay of respiratory chain complexes and genetic analysis. Complex Ⅱ activities decreased in affected tissues. Pathogenic mutations in SDHA gene and SDHAF1 gene encoding assembly factor have been found so far. Clinical treatment aims at improving the mitochondrial function.

Leigh syndrome due to mitochondrial respiratory chain complex II deficiency / 中国当代儿科杂志

Mitochondrial respiratory chain complex II deficiency is a rare documented cause of mitochondrial diseases. This study reported a case of Leigh syndrome due to isolated complex II deficiency. A boy presented with progressive weakness, motor regression and dysphagia after fever from the age of 8 months and hospitalized at the age of 10 months. Elevated blood levels of lactate and pyruvate were observed. Brain magnetic resonance image showed symmetrical lesions in the basal ganglia. Mitochondrial respiratory chain complex I-V activities in peripheral leukocytes were measured using spectrophotometric assay. Mitochondrial gene screening of common point mutations was performed. The complex II activity in the peripheral leukocytes decreased to 21.9 nmol/min per mg mitochondrial protein (control: 47.3±5.3 nmol/min per mg mitochondrial protein). The ratio of complex II activity to citrate synthase activity (22.1%) also decreased (control: 50.9%±10.7 %). No point mutation was found in mitochondrial DNA. The boy was diagnosed as Leigh syndrome due to isolated complex II deficiency. Psychomotor improvements were observed after the treatment. The patient is 22 months old and in a stable condition.

Thiabendazole inhibits ubiquinone reduction activity of mitochondrial respiratory complex II via a water molecule mediated binding feature

The mitochondrial respiratory complex II or succinate: ubiquinone oxidoreductase (SQR) is a key membrane complex in both the tricarboxylic acid cycle and aerobic respiration. Five disinfectant compounds were investigated with their potent inhibition effects on the ubiquinone reduction activity of the porcine mitochondrial SQR by enzymatic assay and crystallography. Crystal structure of the SQR bound with thiabendazole (TBZ) reveals a different inhibitor-binding feature at the ubiquinone binding site where a water molecule plays an important role. The obvious inhibitory effect of TBZ based on the biochemical data (IC(50) ~100 μmol/L) and the significant structure-based binding affinity calculation (~94 μmol/L) draw the suspicion of using TBZ as a good disinfectant compound for nematode infections treatment and fruit storage.

Enzyme analysis of isolated mitochondrial respiratory chain complex III deficiency / 中华儿科杂志

<p><b>OBJECTIVE</b>To study the clinical and enzymological characteristics of the children with mitochondrial respiratory chain complex III deficiency.</p><p><b>METHOD</b>The clinical manifestations of five patients (3 males, 2 females) were summarized. Spectrophotometric assay was used for the analysis of respiratory chain complex I to V enzyme activity in peripheral blood leukocytes, after obtaining venous blood.</p><p><b>RESULT</b>(1) Five patients were hospitalized at the age of 1 month to 15 years. Three patients had Leigh syndrome with progressive motor developmental delay or regression and weakness. One had severe liver damage and intrahepatic cholestasis. One presented muscle weakness. (2) Deficient complex I + III activity was identified in five patients. Their complex I + III activities in peripheral blood leukocytes were 3.0 to 14.2 nmol/min per mg mitochondrial protein (control: 84.4 ± 28.5 nmol/min per mg mitochondrial protein). The ratio of complex I + III to citrate synthase decreased to 3.5 to 22.9% (normal control 66.1 ± 14.7%). The activities of complex III decreased to 10.4 to 49.3% of the lowest control value, while complex I, II, IV and V activities were normal. The results supported the diagnosis of isolated respiratory chain complex III deficiency.</p><p><b>CONCLUSION</b>Complex III deficiency is a kind of disorder of energy metabolism with various manifestations. The complex I + III activities and the ratio of complex I + III to citrate synthase were lower than those of the control. The activities of complex I, II, IV and V were normal.</p>

Determinación por medio de marcadores moleculares SSCP y RAPD de la diversidad genética en la especie Taenia solium en Colombia / Determination by SSPC and RAPD of genetic diversity in Taenia solium especies, main causative agent of teniosis and cysticercosis in Colombia

Utilizando las técnicas moleculares de SSCP y RAPD se pudo evidenciar rápida y claramente la variabilidad genética en Colombia de larvas del céstodo Taenia solium analizando fragmentos de genes de ADN mitocondrial y fragmentos aleatorios de ADN nuclear. El ADN estudiado se obtuvo de ocho aislados de cisticercos de cerdo provenientes de tres departamentos de Colombia: Antioquia, Nariño y Sucre. Los fragmentos obtenidos por PCR de los genes NADH deshidrogenasa 1 (ND1) y citocromo oxidasa c subunidad I (COI) al ser denaturados y analizados en geles no denaturantes de acrilamida, mostraron al menos tres patrones diferentes por cada gen analizado, verificando que estos genes conservados mitocondriales son polimórficos en T. solium colombiana. Por otra parte, los cebadores decaméricos de RAPD produjeron patrones polimórficos, corroboraron la diversidad genética entre los diferentes aislamientos analizados.

Effects of yinxing pingchan recipe and its components on activity of mitochondrial enzyme complex in brain of mice with Parkinson's disease / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To investigate the mechanisms of Yinxing Pingchan recipe (YXPC) and its components, i.e. the components for detoxicating (A), for calming liver (B) and for dissolving blood stasis(C), in preventing and treating Parkinson's disease, and the path of its inhibition on nigrostriatal dopaminergic neuron (DAn) apoptosis in model mice of Parkinson's disease.</p><p><b>METHODS</b>Male C57BL/6J mice were divided into the normal group, the model group and four Chinese medicinal groups, that is, the YXPC group, and Group A, B and C, treated with YXPC and its components A, B and C respectively. Mouse model of Parkinson's disease was established by intraperitoneal injection with 1-methl-4-phenyl-1,2,3,6-tetrahydropyridin (MPTP). All mice were sacrificed in 2 batches at the 14th and the 28th day respectively. The activity of mitochondrial enzyme complex I, II and IV (MEC I, II and IV) in the brain of mice were measured, respectively.</p><p><b>RESULTS</b>As compared with the normal group, the activity of MEC I and IV in brain was significantly lower (P < 0.05 or P < 0.01), and that of MEC II had no obvious change in the model group. As compared with the model group, the activity of MEC I was significantly higher in YXPC group and Group C at the 14th day (P < 0.05), while the activity of MECII in Group A at the 14th day, Group B at the 28th day and Group C at both 14th and 28th day was significantly lower (P<0.05 or P<0.01). Activity of MEC IV in the four Chinese medicinal groups at the 14th day all significantly increased (P<0.05 or P<0.01), and retained at high level in Group B and Group C at the 28th day (P<0.05).</p><p><b>CONCLUSION</b>YXPC and its components can maintain the mitochondrial function by partial inhibiting the activity of its enzyme complex, preventing DAn apoptosis to slow down the progress of Parkinson's disease.</p>