Biomedical subjects

Q Feng

Publications and source records attributed to Q Feng.

At least 37 records · Page 2Linked to original sources

PubMed2001

The ABC transporter Pdr5p mediates the efflux of nonsteroidal ecdysone agonists in Saccharomyces cerevisiae.

We have previously shown that the synthetic nonsteroidal ecdysone agonist tebufenozide (RH-5992) is actively excluded by resistant cells of insects. To identify the transporter that could be involved in the efflux of RH-5992, the role of three ATP binding cassette transporters, Pdr5p, Snq2p and Ycf1p, has been studied using transporter-deletion mutants of yeast Saccharomyces cerevisiae. PDR5 (pleiotropic drug resistance 5) deletion mutants (Deltapdr5 and Deltapdr5Deltasnq2) retained significantly higher levels of 14C-radiolabeled RH-5992 within the cells when compared to wild-type strain or single deletion mutants of SNQ2 (Deltasnq2) and YCF1 (Deltaycf1). Introduction of an expression vector containing the PDR5 gene into the PDR5 single deletion mutant reversed the effect, resulting in the active exclusion of [14C]RH-5992 from these cells as efficiently as the wild-type cells. These results demonstrated that the ABC transporter Pdr5p but not Snq2p or Ycf1p was responsible for the active exclusion of [14C]RH-5992 in yeast. This exclusion was temperature-dependent and was blocked by the ATPase inhibitors oligomycin and vanadate, indicating that the efflux was an active process. The mutants with the PDR5 deletion can also selectively accumulate [14C]RH-0345 and [14C]RH-2485, but not [14C]RH-5849, indicating that these three compounds share the same transporter Pdr5p for efflux.

ATP-Binding Cassette Transporters↗

PubMed2001

Anticarcinogenic antioxidants as inhibitors against intracellular oxidative stress.

Oxidative stress has been implicated in the pathogenesis of numerous diseases, including cancer. In the present study, the protective effect of natural antioxidants, such as quercetin and tea polyphenols, on intracellular oxidative stress was studied. Here we report a novel function of quercetin and tea polyphenols, as potential inhibitors of 4-hydroxy-2-nonenal (HNE)-induced intracellular oxidative stress and cytotoxicity. In rat liver epithelial RL34 cells, a potent electrophile HNE dramatically induced the productions of reactive oxygen species (ROS), which correlated well with the reduction in cell viability. We found that quercetin and tea polyphenols, such as epigallocatechin gallate and theaflavins and their gallate esters, significantly inhibited the HNE-induced ROS production and cytotoxicity. In addition, HNE induced a transient decrease in the mitochondrial membrane potential (delta psi), which was also retarded by the antioxidants. These data suggest that the antioxidants, such as quercetin and tea polyphenols, are inhibitors against mitochondrial ROS production.

Aldehydes↗

PubMed2001

Methylation of the protein phosphatase 2A catalytic subunit is essential for association of Balpha regulatory subunit but not SG2NA, striatin, or polyomavirus middle tumor antigen.

Binding of different regulatory subunits and methylation of the catalytic (C) subunit carboxy-terminal leucine 309 are two important mechanisms by which protein phosphatase 2A (PP2A) can be regulated. In this study, both genetic and biochemical approaches were used to investigate regulation of regulatory subunit binding by C subunit methylation. Monoclonal antibodies selectively recognizing unmethylated C subunit were used to quantitate the methylation status of wild-type and mutant C subunits. Analysis of 13 C subunit mutants showed that both carboxy-terminal and active site residues are important for maintaining methylation in vivo. Severe impairment of methylation invariably led to a dramatic decrease in Balpha subunit binding but not of striatin, SG2NA, or polyomavirus middle tumor antigen (MT) binding. In fact, most unmethylated C subunit mutants showed enhanced binding to striatin and SG2NA. Certain carboxy-terminal mutations decreased Balpha subunit binding without greatly affecting methylation, indicating that Balpha subunit binding is not required for a high steady-state level of C subunit methylation. Demethylation of PP2A in cell lysates with recombinant PP2A methylesterase greatly decreased the amount of C subunit that could be coimmunoprecipitated via the Balpha subunit but not the amount that could be coimmunoprecipitated with Aalpha subunit or MT. When C subunit methylation levels were greatly reduced in vivo, Balpha subunits were found complexed exclusively to methylated C subunits, whereas striatin and SG2NA in the same cells bound both methylated and unmethylated C subunits. Thus, C subunit methylation is critical for assembly of PP2A heterotrimers containing Balpha subunit but not for formation of heterotrimers containing MT, striatin, or SG2NA. These findings suggest that methylation may be able to selectively regulate the association of certain regulatory subunits with the A/C heterodimer.

3T3 Cells↗

PubMed2001

Increased L-arginine uptake and inducible nitric oxide synthase activity in aortas of rats with heart failure.

L-Arginine crosses the cell membrane primarily through the system y(+) transporter. The aim of this study was to investigate the role of L-arginine transport in nitric oxide (NO) production in aortas of rats with heart failure induced by myocardial infarction. Tumor necrosis factor-alpha levels in aortas of rats with heart failure were six times higher than in sham rats (P < 0.01). L-Arginine uptake was increased in aortas of rats with heart failure compared with sham rats (P < 0.01). Cationic amino acid transporter-2B and inducible (i) nitric oxide synthase (NOS) expression were increased in aortas of rats with heart failure compared with sham rats (P < 0.05). Aortic strips from rats with heart failure treated with L-arginine but not D-arginine increased NO production (P < 0.05). The effect of L-arginine on NO production was blocked by L-lysine, a basic amino acid that shares the same system y(+) transporter with L-arginine, and by the NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME). Treatment with L-lysine and L-NAME in vivo decreased plasma nitrate and nitrite levels in rats with heart failure (P < 0.05). Our data demonstrate that NO production is dependent on iNOS activity and L-arginine uptake and suggest that L-arginine transport plays an important role in enhanced NO production in heart failure.

Animals↗

PubMed2001

Cardiac myocytes exposed to anoxia-reoxygenation promote neutrophil transendothelial migration.

The goal of the present study was to assess whether cardiac myocytes exposed to anoxia-reoxygenation (A/R) could generate a chemotactic gradient for polymorphonuclear neutrophil (PMN) transendothelial migration. Exposure of neonatal mouse cardiac myocytes to A/R induced an oxidant stress in the myocytes. Supernatants obtained from A/R-conditioned myocytes promoted mouse PMN migration across mouse myocardial endothelial cell monolayers. This increase in PMN transendothelial migration could be prevented if catalase or a platelet-activating factor (PAF) antagonist was added to the supernatants before assay. Supernatants from A/R-conditioned myocytes activated endothelial cells by inducing an intracellular oxidant stress. The oxidant stress and PMN transendothelial migration induced by supernatants from A/R-conditioned myocytes were substantially reduced when endothelial cells derived from manganese superoxide dismutase overexpressing mice were used in the assays. Supernatants from A/R-conditioned myocytes also increased endothelial cell surface levels of E-selectin and intercellular adhesion molecule-1. Our results indicate that cardiac myocytes exposed to A/R can generate a chemotactic gradient, presumably due to production and release of stable oxidants and PAF. The ability of supernatants from A/R-conditioned myocytes to promote PMN transendothelial migration was largely dependent on induction of an oxidant stress in endothelial cells. In addition, these supernatants also induced a proadhesive phenotype in the endothelial cells.

Animals↗

PubMed2001

A novel method for enzyme immobilization: direct encapsulation of acid phosphatase in nanoporous silica host materials.

Immobilization of acid phosphatase (ACP) in mesoporous or, more generally, nanoporous silica has been accomplished via the sol-gel reactions of tetramethyl orthosilicate in the presence of ACP and of D-glucose (DG) as a nonsurfactant template, which is subsequently removed by water extraction after the formation of nanocomposite gels. Characterization of the silica host after the removal of DG shows that the pore size and volume generally increase with the DG content. At high DG contents, the silica hosts are nanoporous with interconnected nanoscaled pores/channels of regular diameter (e.g., 3.4 nm). Catalytic activity of ACP encapsulated in nanoporous hosts is significantly improved over that in microporous host prepared in the absence of DG. The apparent enzymatic activity at various pH values and substrate concentrations correlates well with the nanostructures of the host matrices. As the DG content is increased in the synthesis, the activity tends to increase. At a DG content of 42-60 wt%, the samples exhibit activities about triple that of the template-free control. These and other results from enzymatic kinetic studies suggest that the increase in the pore size and volume facilitates the transport of the substrate and product molecules in the host matrices, leading to the observed increase in activity. The thermal stability of ACP is remarkably improved upon immobilization. There is no detectable leakage of ACP from the host matrices and the biogels are reuseable. This study provides a useful protocol for the development of nanotechnology for various biocatalysts and biosensors.

Acid Phosphatase↗

PubMed2001

Human ovarian cancer and cisplatin resistance: possible role of inhibitor of apoptosis proteins.

The inhibitor of apoptosis proteins (IAPs) constitutes a family of highly conserved apoptosis suppressor proteins that were originally identified in baculoviruses. Although IAP homologs have recently been demonstrated to suppress apoptosis in mammalian cells, their expression and role in human ovarian epithelial cancer and chemotherapy resistance are unknown. In the present study we used cisplatin-sensitive and -resistant human ovarian surface epithelial (hOSE) cancer cell lines and adenoviral antisense and sense complementary DNA expression to examine the role of IAP in the regulation of apoptosis in human ovarian cancer cells and chemoresistance. Antisense down-regulation of X-linked inhibitor of apoptosis protein (Xiap), but not human inhibitor of apoptosis protein-2 (Hiap-2), induced apoptosis in cisplatin-sensitive and, to a lesser extent, in -resistant cells. Cisplatin consistently decreased Xiap content and induced apoptosis in the cisplatin-sensitive, but not cisplatin-resistant, cells. Hiap-2 expression was either unaffected or inhibited to a lesser extent. The inhibition of IAP protein expression and induction of apoptosis by cisplatin was time and concentration dependent. Infection of cisplatin-sensitive cells with adenoviral sense Xiap complementary DNA resulted in overexpression of Xiap and markedly attenuated the ability of cisplatin to induce apoptosis. Immunohistochemical localization of the IAPs in hOSE tumors demonstrated the presence of Xiap and Hiap-2, with their levels being highest in proliferative, but not apoptotic, epithelial cells. These studies indicate that Xiap is an important element in the control of ovarian tumor growth and may be a point of regulation for cisplatin in the induction of apoptosis. These results suggest that the ability of cisplatin to down-regulate Xiap content may be an important determinant of chemosensitivity in hOSE cancer.

Aged↗

PubMed2001

Attenuation of compensatory right ventricular hypertrophy and heart failure following monocrotaline-induced pulmonary vascular injury by the Na+-H+ exchange inhibitor cariporide.

Pulmonary hypertension results in compensatory right ventricular (RV) hypertrophy. We studied the role of the Na+-H+ exchange (NHE) in the latter process by determining the effect of the NHE-1 inhibitor cariporide after monocrotaline-induced pulmonary artery injury. Sprague-Dawley rats received a control or cariporide diet for 7 days, at which time they were administered either monocrotaline (60 mg/kg) or its vehicle. Twenty-one days later, monocrotaline control, but not cariporide-fed animals, demonstrated increased RV weights and cell size of 65 and 52%, respectively. Monocrotaline alone significantly increased RV systolic pressure and end diastolic pressure by 70 and 94%, respectively, whereas corresponding values with cariporide were significantly reduced to 33 and 42%. Central venous pressure increased by 414% in control animals, which was significantly reduced by cariporide. Monocrotaline treatment produced a decrease in cardiac output of 28 and 8% in the absence or presence of cariporide (P < 0.05 between groups), respectively. Although body weights were significantly lower in both monocrotaline-treated groups compared with vehicle treatment, with cariporide the net gain in body weight was twice that seen in the monocrotaline-treated animals without cariporide. Monocrotaline also increased RV NHE-1 and atrial natriuretic peptide mRNA expression, which was abrogated by cariporide. Monocrotaline-induced myocardial necrosis, fibrosis, and mononuclear infiltration was completely prevented by cariporide. Cariporide had no effect on monocrotaline-induced pulmonary intimal wall thickening. Our results demonstrate that cariporide directly attenuates myocardial dysfunction after monocrotaline administration independent of pulmonary vascular effects. NHE-1 inhibition may represent an effective adjunctive therapy that selectively targets myocardial hypertrophic responses in pulmonary vascular injury.

Animals↗

PubMed2000

A Saccharomyces gene family involved in invasive growth, cell-cell adhesion, and mating.

The cell wall of bakers' yeast contains a family of glycosyl-phosphatidylinositol (GPI)-linked glycoproteins of domain structure similar to the adhesins of pathogenic fungi. In wild-type cells each of these proteins has a unique function in different developmental processes (mating, invasive growth, cell-cell adhesion, or filamentation). What unifies these developmental events is adhesion, either to an inert substrate or to a cell. Although they differ in their specificities, many of these proteins can substitute for each other when overexpressed. For example, Flo11p is required during vegetative growth for haploid invasion and diploid filamentation, whereas Fig2p is required for mating. When overexpressed, Flo11p and Fig2p can function in mating, invasion, filamentation, and flocculation. The ability of Flo11p to supply Fig2p function in mating depends on its intracellular localization to the mating projection, where Fig2p normally functions in the adhesion of mating cells. Our data show that even distant family members retain the ability to carry out disparate functions if localized and expressed appropriately.

Cell Adhesion↗

PubMed2000

Tumor necrosis factor-alpha induces apoptosis via inducible nitric oxide synthase in neonatal mouse cardiomyocytes.

OBJECTIVE: It has been demonstrated that tumor necrosis factor-alpha (TNF alpha) induces apoptosis in cardiac myocytes. However, its mechanism of action is still not well understood. In the present study, we hypothesized that TNF alpha induces myocardial apoptosis by induction of inducible nitric oxide synthase (iNOS). METHODS: Neonatal cardiac myocytes were isolated from iNOS (-/-) mutant and C57BL6 wild type mice. Cells were cultured for 3 days before treatment with an NO donor or TNF alpha. Following treatment with S-nitroso-N-acetyl-penicillamine (SNAP) or TNF-alpha, cells were tested for apoptosis by terminal deoxynucleotidyl transfer-mediated end labeling (TUNEL) staining and cell death detection ELISA. NO production was measured by nitrite concentration in the culture medium. Cardiomyocyte expression of iNOS and TNF type 1 receptor (TNFR1) mRNA was determined by reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: SNAP (0.01-100 microM) induced apoptosis of cardiac myocytes in a concentration-dependent manner in the wild type mice (n = 5, P < 0.01). TNFR1 mRNA was expressed in neonatal cardiomyocytes from both wild type and iNOS (-/-) mutant mice. TNF alpha induced a concentration-dependent increase in iNOS mRNA expression and nitrite production as well as significant apoptosis of cardiomyocytes in the wild type mice (n = 4, P < 0.01). However, without iNOS expression, the apoptotic effects of TNF-alpha were significantly attenuated in cardiomyocytes from iNOS (-/-) mutant mice (n = 4, P < 0.05). CONCLUSION: TNF alpha induces apoptosis via iNOS expression and NO production in neonatal mouse cardiomyocytes.

Analysis of Variance↗

PubMed2000

Venous neuropeptide Y receptor responsiveness in patients with chronic heart failure.

BACKGROUND: Chronic heart failure is associated with increased sympathetic nerve activity and elevated plasma neuropeptide Y levels. The aim of this study was to investigate whether increased neuropeptide Y release altered vascular neuropeptide Y responses in the dorsal hand veins in patients with chronic heart failure. METHODS AND RESULTS: Neuropeptide Y responsiveness was studied in vivo with use of a hand vein tonometry technique in 14 patients with chronic heart failure and left ventricular ejection fraction (LVEF) values <20%, 16 patients with LVEF values from 20% to 35%, and 16 age-similar healthy control subjects. Plasma norepinephrine and neuropeptide Y levels were significantly elevated in patients with chronic heart failure and LVEF values <20% compared with control subjects (P < .01). Plasma neuropeptide Y but not norepinephrine levels were significantly elevated in patients with chronic heart failure and LVEF values from 20% to 35% compared with control subjects (P < .01). Increasing doses of neuropeptide Y (25 to 2,000 pmol/min) were infused into a dorsal hand vein of each subject. Dose-dependent venoconstriction to neuropeptide Y was observed in all subjects studied. The neuropeptide Y dose-response curve in patients with LVEF values from 20% to 35% was significantly shifted to the left compared with patients with LVEF values <20% and control subjects (P < .01), whereas no significant difference was observed between the control subjects and the patients with LVEF values <20%. No significant difference in neuropeptide Y dose responses was observed between patients with chronic heart failure with plasma neuropeptide Y levels above the median and patients with chronic heart failure with plasma neuropeptide Y levels below the median. CONCLUSIONS: In vivo venous neuropeptide Y receptor responsiveness is increased in patients with chronic heart failure and LVEF values from 20% to 35%. This increased neuropeptide Y responsiveness may contribute to venoconstriction at this stage of heart failure.

Cardiac Output, Low↗

PubMed2000

Long-term effects of cis and trans monounsaturated (18:1) and saturated (16:0) fatty acids on the synthesis and secretion of apolipoprotein A-I- and apolipoprotein B-containing lipoproteins in HepG2 cells.

The objective of this study was to compare the long-term effects of oleic (cis 18:1), elaidic (trans 18:1), and palmitic (16:0) acids on hepatic lipoprotein production, using HepG2 cells as an experimental model. The net accumulation in the medium of apolipoprotein A-I (apoA-I) was not significantly altered by fatty acids, whereas that of apoB was increased with oleic and elaidic acids. Oleic acid, and to a lesser extent elaidic and palmitic acids, increased the mass of triglycerides in the medium and the incorporation of [(3)H]glycerol into secreted triglycerides. The incorporation of [(14)C]acetate into cellular and secreted total cholesterol was stimulated by 96% and 83%, respectively, with elaidic acid but was not significantly modified by oleic or palmitic acid. Relative to oleic acid, the secretion of (14)C-labeled phospholipids and triglycerides was decreased 28% to 31% with elaidic and palmitic acids whereas that of free cholesterol and cholesteryl esters was enhanced 93% and 73%, respectively, with elaidic acid but remained unchanged with palmitic acid. Compared with oleic acid, elaidic acid stimulated the secretion of very low density lipoprotein cholesterol (VLDL-Chol), low density lipoprotein cholesterol (LDL-Chol), and high density lipoprotein cholesterol (HDL-Chol) by 43%, 70%, and 34%, respectively, whereas palmitic acid decreased VLDL-Chol but had no significant effect on LDL-Chol and HDL-Chol. The ratios of total cholesterol to HDL-Chol were 3.17, 3.60, and 3.25 with oleic, elaidic, and palmitic acids, respectively; the corresponding ratios of LDL-Chol to HDL-Chol were 0.87, 1.10, and 0.93, respectively. Compared with oleic and palmitic acids, the LDL and HDL particles secreted in the presence of elaidic acid contained higher levels of free cholesterol and cholesteryl esters and a lower content of phospholipids. The phospholipid-to-total cholesterol ratios of HDL were 1.05, 0.40, and 0.76 with oleic, elaidic, and palmitic acids, respectively. Our results indicate that in comparison with cis monounsaturated and saturated fatty acids, trans fatty acids have more adverse effects on the concentration and composition of lipoproteins secreted by HepG2 cells.

Apolipoprotein A-I↗

PubMed2000

[Clinical significance of beta-hCG and human placental lactogen in serum of normal pregnancies and patients with pregnancy induced hypertension].

OBJECTIVE: To examine the level of beta-hCG and Human Placental Lactogen (HPL) in maternal serum of normal pregnancies and patients with pregnancy induced hypertension (PIH) and to study the clinical significance and effects of them on the pathogenesis of the disease. METHODS: Serum levels of beta-hCG and HPL of 142 normal pregnant women and 43 patients with PIH (16 mild, 12 moderate and 15 severe) were determined by radioimmunossay. RESULTS: (1) Serum levels of beta-hCG in all PIH subgroups [(25.33 +/- 17.80) micrograms/L in mild, (33.12 +/- 4.91) micrograms/L in moderate, (42.19 +/- 17.47) micrograms/L in severe] were significantly higher than the normal pregnant group [(12.33 +/- 7.92) micrograms/L; P < 0.001]. There is positive correlation between levels of beta-hCG and degrees of PIH (r = 0.677, P < 0.05). (2) Serum levels of HPL in all PIH subgroups [(14.73 +/- 3.26) mg/L in mild, (11.44 +/- 4.02) mg/L in moderate, (12.73 +/- 4.18) mg/L in severe] did not show significant difference when compared with that of normal pregnant group [(12.78 +/- 4.67) mg/L; P > 0.05]. Furthermore, there was no correlation between levels of HPL and degrees of PIH (r = -0.300, P > 0.05). CONCLUSIONS: Serum beta-hCG could reflect the degree of functional imbalance of the placental trophoblasts on PIH and it may be used as a clinical detecting index of PIH. On the other hand, HPL is not such a useful factor.

Adult↗

PubMed2000

[Ligand of platelet and T cell activation antigen 1 (PTA1) expressed on Colo205 cell surface].

OBJECTIVE: To confirm the existence of PTA1 ligand (PTA1L). METHODS: PTA1/Ig fusion protein was prepared by gene recombination and expression in COS-7 cells by DEAE-dextran transfection. The fusion protein was used as a probe in the investigation of PTA1L by immunohistochemical staining. Existence of PTA1L was further identified by adhesion experiment. RESULTS: Colo205 cells could be stained by PTA1/Ig fusion protein specifically but not by hIg, and the adhesion of activated Jurkat cells with Colo205 could be blocked by PTA1/Ig and PTA1 mAb. CONCLUSION: PTA1 ligand is present on the surface of Colo205 cells. These results provide a solid basis for further investigation of the role of PTA1-PTA1L interaction in the pathogenesis of neoplasm.

Animals↗

PubMed2000

[Study on the in vitro cleavage abilities of ribozymes specific to different sites of bcr-abl fusion gene and their induction of apoptosis in K562 cells].

OBJECTIVE: To investigate the in vitro cleavage abilities of ribozymes specific to different sites of bcr-abl fusion gene and their effects on K562 cell. METHODS: First, three single-ribozymes specific to the fusion point were designed. After recombination, 6 vectors including single-, double- and triple- ribozymes were constructed and their in vitro cleavage abilities were compared. Then the triple-unit ribozyme retroviral vector was transfected into K562 cell to test its effect on cell cycle, apoptosis and cell structure. RESULTS: These ribozymes can cleave the template in vitro with different efficiency. The triple-unit ribozyme, with an efficiency of 70.8%, was the most efficient one. The cleavage efficiency of single-unit RZ1, RZ2 and RZ3 was 54.6%, 25.3% and 3.6%, respectively. Those of double-unit RZ12 and RZ23 were 60.7% and 30.3% respectively. The triple-unit ribozyme could inhibit the K562 cell growth by inducing apoptosis. CONCLUSION: It is a new way to treat CML by ribozymes specific to bcr-abl fusion gene, which made it available to purge bone marrow by bcr-abl specific ribozymes.

Apoptosis↗

PubMed2000

[A comparative study on the expressions of IL-4, IFN-gamma and TNF-alpha in BMMNC of acute and chronic aplastic anemia patients].

OBJECTIVE: To detect the induced levels of IL-4, IFN-gamma and TNF-alpha in the supernatant of bone marrow mononuclear cells (BMMNC) and compare the difference of immune status between acute (SAA) and chronic (CAA) aplastic anemia patients. METHODS: Concentrations of IL-4, IFN-gamma and TNF-alpha in PHA-P-induced BMMNC supernatants were determined by ELISA assay in 11 SAA and 13 CAA patients as well as 16 controls. Concentration differences between the two groups were compared. RESULTS: (1) The IFN-gamma and TNF-alpha levels in AA patients studied were much higher than that in controls, and IL-4 levels were normal in SAA group but elevated in CAA group. (2) TNF-alpha levels were comparable between the two AA groups, but both IL-4 and IFN-gamma levels were significantly different between them. CONCLUSION: Enhanced cellular immunity seems to play an important role in the pathogenesis of SAA, and enhancement of both cellular and humoral immunity might contribute to the pathogenesis of CAA.

Acute Disease↗

PubMed2000

[Studies on the effect-increasing components for molluscacides in nut of Areca catech L].

OBJECTIVE: To investigate the effect-increasing action of Areca catech for molluscacide. METHOD: Experiments were conducted on the effect-increasing components isolated from the dry nut of A. catech. RESULT: Arecoline has been proved the most effect-increasing component. CONCLUSION: When used with SPA arecoline could reduce markedly the doses of the two agents.

Animals↗

PubMed2000

[Studies on metal porphyrins as two-functional mimic of enzyme].

In this study, four metal porphyrins (tetraphenylporphyrinesulfonatoiron, tetraphenylporphyrinesulfon-atocopper, tetraphenylporphyrinesulfonatomanganese, and tetraphenyl porrphyrinesulfonatocobalt) were used as dual function mimicry of superoxide dismutase (SOD) and catalase (CAT). The first function, scavenging O2.-, has been proved by using riboflavine-methionine photoreduction method in the concentration range of 10(-5)-10(-6) mol/L. The second function, scavenging H2O2, has been demonstrated by means of spectrophotometry, and the percentage of decomposing H2O2 increases with the concentration of the imitating compounds. Metal porphyrins, SOD and CAT were measured by the liver homogenate technique of mice and the results showed that they had obvious action of decreasing the lipid peroxidation. Tetraphenylporphyrinesulfonatomanganese was measured by isolated ischemia reperfusion heart of rats. The results indicated that the Mn-TPPS4 could reduce the damages of active oxygen and had evidently protective effects on isolated ischemia-reperfusion mocardium of rats.

Animals↗