Enhanced production of manganese peroxidase by Phanerochaete chrysosporium

Production of manganese-dependent peroxidase (MnP) by the white-rot fungus Phanerochaete chrysosporium BKM-F-1767 (ATCC 24725) was monitored during growth in different media and growth conditions. The effect of some activators of MnP production, Mn2+, Tween 80, phenylmethylsulphonylfloride (PMSF), oxygen, temperature, pH, glycerol and nitrogen was studied. Supplementing the cultures with Tween 80 (0.05 percent, v/v) and Mn2+ (174 µM) resulted a maximum MnP activity of 356 U/L which was approximately two times higher than that obtained in the control culture (without Tween 80). Decolourisation of Direct Blue 15 and Direct Green 6 (50 mg/L) was also achieved with MnP.

Protection of Mn~(2+) on Injury of human kidney tubular epithelial cell line induced by bentamicin / 中国临床药理学与治疗学

AIM: To evaluate the protection of Mn~(2+) on injury of human kidney tubular epithelial cell line induced by gentamicin, and investigate its principals. METHODS: Gentamicin was used to injury human kidney tubular epithelial cell line (HK-2) to produce model of kidney injury. MTT method was used to measure effect of Mn~(2+) on proliferation of cells after they were injured by gentamicin. The spectrophotometry method was used to observe the change of LDH,NAG and SOD effected by Mn~(2+). Ultrastructure was examined by electron microscopy. RESULTS: Although HK-2 cells were injured, Mn~(2+) promoted cells proliferation, decreased LDH activity and NAG content, increased SOD activity, and alleviated dilation of the mitochondria and crushing of lysosomes. CONCLUSION: Mn~(2+) can protect human kidney tubular epithelial cell line from injury induced by gentamicin. It may be in relation to inhibiting the oxidative injury, lightening dilation of the mitochondria, protecting the integrity of lysosomes and decrease the leakage of enzyme.

Role of Ca2+ influx in the tert-butyl hydroperoxide-induced apoptosis of HepG2 human hepatoblastoma cellse

Oxidative stress appears to be implicated in the pathogenesis of various diseases including alcoholic liver injury. In this study we investigated the mechanism of apoptosis induced by tert-butyl hydroperoxide (TBHP) in HepG2 human hepatoblastoma cells. Treatment with TBHP significantly reduced glutathione content and glutathione reductase activity, and increased glutathione peroxidase activity, indicating that TBHP induced oxidative stress in the HepG2 cells. TBHP also induced reduction of cell viability and DNA fragmentation, a hallmark of apoptosis, in a dose-dependent manner. In addition, TBHP induced a sustained increase in intracellular Ca2+ concentration, which was completely prevented by the extracellular Ca2+ chelation with EGTA. TBHP also induced Mn2+ influx. These results indicate that the intracellular Ca2+ increase by TBHP is exclusively due to Ca2+ influx from the extracellular site. Treatment with either an extracellular (EGTA) or an intracellular Ca2+ chelator (BAPTA/AM) significantly suppressed the TBHP-induced apoptosis. Taken together, these results suggest that TBHP induced the apoptotic cell death in the HepG2 cells and that Ca2+ influx may play an important role in the apoptosis induced by TBHP.

Effects of Cu~(2+), Zn~(2+) and Mn~(2+)on postsynaptic sites / 中国药理学通报

Effects of Cu2+,Zn2+and Mn2+ on responses to ACh were studied with toad rec-tus abdominis. Cu2+, Zn2+and Mn2+concentra-tion- dependently shifted the concentration-response curves for ACh to the right unparallelly and reduced the maximal response considerably. The pAh values of Cu2+ , Zn2+ and Mn2+ were 3.69, 2.95 and 2. 62, respectively. The inhibitory potent of Cu2+ and Zn2+ seemed to be 11.7 times and 2. 1 times respectively more thanthat of Mn2+. It was suggested that Cu2+, Zn2+ and Mn2+postsynaptically interfere with the action of ACh. However, Zn2+in lower concentration shifted the bottom section of the curve for ACh to the left and top, and shifted the top section of the curve to the right, suggesting that Mn2+in lower concentration be possessed of partial agonistic property.