Effect of uridine on mitochondrial function / 生物工程学报

Uridine is one of the essential nutrients in organisms. To maintain normal cell growth and intracellular metabolism, the uridine must be maintained at certain concentration. Recent studies have shown that uridine can reduce inflammatory response in organisms, participate in glycolysis, and regulate intracellular protein modification, such as glycosylation and acetylation. Furthermore, it can protect cells from hypoxic injury by reducing intracellular oxidative stress, promoting high-energy compounds synthesis. Previous studies have shown that the protective effects of uridine are closely related to its effect on mitochondria. This review summarizes the effect of uridine on mitochondrial function.

Studies on the effect of intratesticular administration of opioid peptides, naloxone or N-acetyl beta-endorphin antiserum on some testicular parameters in rats.

Opioid peptides have been localized in a variety of peripheral tissues like placenta, thyroid, pancreas, gastrointestinal tract, in the reproductive tract of male and female and in the testes of rats. Immunoassayable material was detected in extracts of gonads, reproductive tract and accessory reproductive organs. Studies with naloxone have suggested that beta-endorphin may have an important role in steroidogenesis and may have a role in regulating transport of luminal material. In our studies met-enkephalin, beta-endorphin, naloxone or N-acetyl beta-endorphin antiserum were microinjected intra testicularly once on alternate days for one week and autopsied 24 h after the last injection. Intratesticular administration of 25, 50 and 100 micrograms doses of naloxone induced significant decrease in in vitro secretion of testosterone per se, which was significantly greater with 50 micrograms dose than with those of the other two doses. A 25 micrograms dose had no effect on hyaluronidase or acid phosphatase activity while 50 micrograms dose significantly decreased the enzyme activity. One hundred micrograms dose also significantly decreased hyaluronidase activity. Intratesticular injection of 10 micrograms met-enkephalin or 1 microgram beta-endorphin significantly decreased hyaluronidase activity whereas 20 microliters N-acetyl beta-endorphin antiserum increased the specific activity of hyaluronidase. There was no change in the weight of the testes on treatment with the above agents.

Appearance and persistence of 113-hydroxypregnant-1, 4-diene-3, 20-dione (delta HOP) effect in vivo

Se estudió el efecto "in vitro" de la 11ß-hidroxipregna-1,4-diene-3,20 diona (DeltaHOP) en ratones tratados en forma aguda y crónica con el esteroide, en conparación con los tratados con dexametasona y vehículo. En los experimentos agudos, una inyección de DeltaHOP de 2 mg/100 gm de peso animal tuvo su máximo efecto inhibitorio en la incorporación de uridina-H3 por los timocitos después de 18 h, desapareciendo el efecto a las 36 h, no observándose cambios en los niveles de corticosterona plasmática. Una dosis de 0.033 mg/100 gm de peso animal de dexametasona produjo inhibición en la incorporación de uridina 5 h después de la inyección, juntamente con una disminución significativa de los niveles de corticosterona plasmática; este efecto desapereció a las 12 h, mientras que el ejercido sobre el timo recién desapareció a las 24 h. En el tratamiento crónico DeltaHOP produjo la máxima inhibición 5 h después de la última inyección y se mantuvo hasta las 36 h sin modificar la corticosterona plasmática. En cambio la dexametasona produjo la misma inhibición que DeltaHOP, pero el efecto desapareció antes ( a las 18 h); en estos animales la corticosterona se mantuvo baja hasta las 18 h. En tratamientos crónicos, después de 5 h de la última inyección, DeltaHOP no modificó los pesos de timos y bazos, pero éstos disminuyeron significativamente con el tratamiento de dexametasona. Estos resultados sugieren que la acción "in vivo" de DeltaHOP es diferente a la de los glucocorticoides

Ultrastructural and Autoradiographic Studies of the Effect of Aflatoxin G1 on Hepatic Cells

To investigate toxicity of aflatoxin Gl and its mechanism, light microscopic, histochemical, electron microscopic and autoradiographic studies were done on the rat liver at various time intervals after the administration of aflatoxin Gl. Light microscopic alteration was first observed at 6 hours and necrosis of periportal hepatic cells was found at 18 hours. However, reduction of Feulgen positivity of the nucleus and pyroninophilia of cytoplasm was observed as early as 1 hour. Ultrastructural changes were noted at 6 hours and were advanced at l8 hours. Early changes consisted of nucleolar segregation, dilatation of rough endoplasmic reticulum, swelling of mitochondria and detachment of membrane bound ribosomes followed later by disruption of cytoplasmic organellae and focal necrosis. These changes were most marked at periportal region. Autoradiographic studies showed inhibition of H3-uridine incorporation into the nucleus at 1 hour, was most marked at 6 hours, and showed some recovery at 18 hours. H3-uridine labeling in the cytoplasm was also inhibited and the most marked inhibition was noted at 1 hour after the aflatoxin administration. These data indicate aflatoxin Gi has a hepatotoxic effect, particulary at the periportal region. This toxic effect is likely due to inhibition of nuclear RNA synthesis which leads to inhibition of ribosomal RNA and eventually protein synthesis. The DNA synthesis is also inhibited, as shown by reduction of Feulgen reaction in the nucleus.