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In vitro synthesis of superoxide dismutases of rat liver.

AB - We have previously demonstrated that the activity of superoxide dismutase (SOD), an antioxidant, is enhanced by low-dose X-ray irradiation in various organs of animals such as rats. Since SOD is an enzyme that mediates the dismutation of O2- to H2O2, the question as to whether the resultant H2O2 is further detoxicated into H2O and O2 or not must still be evaluated. Hence, we studied the effect of low-dose X-ray irradiation on the synthesis of glutathione peroxidase (GSHPx), which is an antioxidant that catalyzes this reaction. The results suggest that H2O2 produced by increased SOD activity can be detoxicated into H2O and O2 due to simultaneous enhancement of the GSHPx activity by X-ray irradiation at 20 cGy, in contrast to irradiation at 400 cGy. The results also show the enhancement in enzyme activities by induction of their synthesis shortly after irradiation at 20 cGy. Moreover, as this phenomenon was observed in BALB/c mice (which are more radiation-sensitive compared to other mouse strains) and radiation-resistant C57BL/6NJcl mice, it was considered to be a common phenomenon in the rat spleen. Copyright (C) 1998 Elsevier Science B.V.

Synthesis of Superoxide Dismutase (SOD) Enzyme Mimetics. A Bioinorganic Laboratory Experiment

N2 - We have previously demonstrated that the activity of superoxide dismutase (SOD), an antioxidant, is enhanced by low-dose X-ray irradiation in various organs of animals such as rats. Since SOD is an enzyme that mediates the dismutation of O2- to H2O2, the question as to whether the resultant H2O2 is further detoxicated into H2O and O2 or not must still be evaluated. Hence, we studied the effect of low-dose X-ray irradiation on the synthesis of glutathione peroxidase (GSHPx), which is an antioxidant that catalyzes this reaction. The results suggest that H2O2 produced by increased SOD activity can be detoxicated into H2O and O2 due to simultaneous enhancement of the GSHPx activity by X-ray irradiation at 20 cGy, in contrast to irradiation at 400 cGy. The results also show the enhancement in enzyme activities by induction of their synthesis shortly after irradiation at 20 cGy. Moreover, as this phenomenon was observed in BALB/c mice (which are more radiation-sensitive compared to other mouse strains) and radiation-resistant C57BL/6NJcl mice, it was considered to be a common phenomenon in the rat spleen. Copyright (C) 1998 Elsevier Science B.V.

Synthesis, structure and superoxide dismutase activity …

T1 - Change of glutathione peroxidase synthesis along with that of superoxide dismutase synthesis in mice spleens after low-dose X-ray irradiation

Conventionally synthesised Mn-superoxide dismutase mimics have a multilayer sheet structure with uncontrolled shape, which wastes resources and has a low catalytic efficiency. Here, a bionic-enzyme hyperbranched polyester (HBPE-AMPA-Mn2+) has been synthesised by a self-assembly technique. Results indicate that an electrochemical biosensor based on HBPE-AMPA-Mn2+ particles has excellent electrochemical performance.

Conjugates of superoxide dismutase 1 with amphiphilic …

We have previously demonstrated that the activity of superoxide dismutase (SOD), an antioxidant, is enhanced by low-dose X-ray irradiation in various organs of animals such as rats. Since SOD is an enzyme that mediates the dismutation of O2- to H2O2, the question as to whether the resultant H2O2 is further detoxicated into H2O and O2 or not must still be evaluated. Hence, we studied the effect of low-dose X-ray irradiation on the synthesis of glutathione peroxidase (GSHPx), which is an antioxidant that catalyzes this reaction. The results suggest that H2O2 produced by increased SOD activity can be detoxicated into H2O and O2 due to simultaneous enhancement of the GSHPx activity by X-ray irradiation at 20 cGy, in contrast to irradiation at 400 cGy. The results also show the enhancement in enzyme activities by induction of their synthesis shortly after irradiation at 20 cGy. Moreover, as this phenomenon was observed in BALB/c mice (which are more radiation-sensitive compared to other mouse strains) and radiation-resistant C57BL/6NJcl mice, it was considered to be a common phenomenon in the rat spleen. Copyright (C) 1998 Elsevier Science B.V.

T1 - Synthesis, catalase, superoxide dismutase and antitumour activities of copper(II) carboxylate complexes incorporating benzimidazole, 1,10-phenanthroline and bipyridine ligands

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Regulation of the synthesis of superoxide dismutase …

N2 - We have shown that the cytotoxic response of TNF-sensitive L929 cells and TNF-resistant EMT-6 cells to TNF-α can be modulated by ADP-ribosylation inhibitors independently of ADP-ribosylation rates. To explore the possibility that these inhibitors modulate TNF cytotoxicity by interfering with cellular protective mechanisms, we evaluated their effects on general RNA synthesis and on mRNA expression of two proposed protective genes, manganous superoxide dismutase (MnSOD) and heat shock protein 70 (hsp70). We found that ADP-ribosylation inhibitors could inhibit general RNA synthesis in a dose-dependent fashion to a similar extent in both EMT-6 and L929 cells, although these inhibitors increased or decreased the sensitivity of the cells to TNF, respectively. In EMT-6 cells, combination of actinomycin D with these inhibitors further inhibited the RNA synthesis rate, and it actually decreased the TNF sensitivity of the EMT-6 cells. Furthermore, the expression of MnSOD or hsp70 was not regulated by these inhibitors. Thus, TNF resistance must depend on other mechanisms in addition to the expression of these protective genes.

Induction of manganese superoxide dismutase mRNA …

T1 - ADP-ribosylation inhibitors inhibit cellular RNA synthesis but do not affect expression of manganous superoxide dismutase or heat shock protein 70 in tumor necrosis factor α-sensitive and -resistant tumor cells

Synthesis, superoxide dismutase mimetic and …

We have shown that the cytotoxic response of TNF-sensitive L929 cells and TNF-resistant EMT-6 cells to TNF-α can be modulated by ADP-ribosylation inhibitors independently of ADP-ribosylation rates. To explore the possibility that these inhibitors modulate TNF cytotoxicity by interfering with cellular protective mechanisms, we evaluated their effects on general RNA synthesis and on mRNA expression of two proposed protective genes, manganous superoxide dismutase (MnSOD) and heat shock protein 70 (hsp70). We found that ADP-ribosylation inhibitors could inhibit general RNA synthesis in a dose-dependent fashion to a similar extent in both EMT-6 and L929 cells, although these inhibitors increased or decreased the sensitivity of the cells to TNF, respectively. In EMT-6 cells, combination of actinomycin D with these inhibitors further inhibited the RNA synthesis rate, and it actually decreased the TNF sensitivity of the EMT-6 cells. Furthermore, the expression of MnSOD or hsp70 was not regulated by these inhibitors. Thus, TNF resistance must depend on other mechanisms in addition to the expression of these protective genes.

Synthesis, catalase, superoxide dismutase and …

AB - We have shown that the cytotoxic response of TNF-sensitive L929 cells and TNF-resistant EMT-6 cells to TNF-α can be modulated by ADP-ribosylation inhibitors independently of ADP-ribosylation rates. To explore the possibility that these inhibitors modulate TNF cytotoxicity by interfering with cellular protective mechanisms, we evaluated their effects on general RNA synthesis and on mRNA expression of two proposed protective genes, manganous superoxide dismutase (MnSOD) and heat shock protein 70 (hsp70). We found that ADP-ribosylation inhibitors could inhibit general RNA synthesis in a dose-dependent fashion to a similar extent in both EMT-6 and L929 cells, although these inhibitors increased or decreased the sensitivity of the cells to TNF, respectively. In EMT-6 cells, combination of actinomycin D with these inhibitors further inhibited the RNA synthesis rate, and it actually decreased the TNF sensitivity of the EMT-6 cells. Furthermore, the expression of MnSOD or hsp70 was not regulated by these inhibitors. Thus, TNF resistance must depend on other mechanisms in addition to the expression of these protective genes.

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