Increase in manganese superoxide dismutase activity in the mouse heart after X-irradiation

Oberley, Larry W.; Clair, Daret K. St; Autor, Anne P.; Oberley, Terry D.

doi:10.1016/0003-9861(87)90082-8

Cited by 156 publications

(70 citation statements)

References 27 publications

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“…The role of MnSOD in this issue is, however, complicated because there is powerful evidence to suggest that MnSOD is antiproliferative in malignant cells (Oberley and Oberley, 1997). It has been shown that transfection of the MnSOD gene leads to a suppression of the malignant phenotype and decreased cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

“…Its pathogenesis has been postulated to be associated with the generation of free radicals (Kamp et al, 1992;Mossman et al, 1996). In contrast to previous observations, which have shown that MnSOD is usually low in malignant tumours (Oberley and Buettner, 1979;Oberley and Oberley, 1997), we have recently shown that the mRNA level, immunoreactive protein and specific activity of MnSOD are highly expressed in the tumour cells of malignant mesotheliomas when compared to healthy pleura or non-malignant transformed human mesothelial cells (Met5A) (Kinnula et al, 1996;Kahlos et al, 1998). Mesothelioma is resistant to cytotoxic drugs and radiation, both of which are known to induce generation of ROS (Sinha and Mimnaugh, 1990;Nakano et al, 1996).…”

mentioning

confidence: 85%

“…The results of the present study confirm our earlier finding on elevated MnSOD activity in M38K cells as compared to Met5A cells (Kinnula et al, 1996), the specific activity of MnSOD being 36.0 ± 3.4 U mg -1 protein in M38K cells and 1.8 ± 1.0 U mg -1 protein in Met5A cells. Moreover, the activities of the mitochondrial enzymes citrate synthase and cytochrome c oxidase, which have been used as constitutive mitochondrial enzymes (Freeman et al, 1986;Oberley et al, 1987;Vuorinen et al, 1995), did not differ significantly between the two cell lines. The activity of citrate synthase was 45.9 ± 5.3 nmol min -1 mg -1 protein in M38K cells and 32.7 ± 10.7 nmol min -1 mg -1 protein in Met5A cells (P = 0.127), the corresponding activities for cytochrome c oxidase being 3.2 ± 1.0 and 2.4 ± 0.9 nmol min -1 mg -1 protein (P = 0.340).…”

Section: Mnsod Citrate Synthase and Cytochrome C Oxidasementioning

confidence: 99%

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Generation of reactive oxygen species by human mesothelioma cells

et al. 1999

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Malignant mesothelioma cells contain elevated levels of manganese superoxide dismutase (MnSOD) and are highly resistant to oxidants compared to non-malignant mesothelial cells. Since the level of cellular free radicals may be important for cell survival, we hypothesized that the increase of MnSOD in the mitochondria of mesothelioma cells may alter the free radical levels of these organelles. First, MnSOD activity was compared to the activities of two constitutive mitochondrial enzymes; MnSOD activity was 20 times higher in the mesothelioma cells than in the mesothelial cells, whereas the activities of citrate synthase and cytochrome c oxidase did not differ significantly in the two cell lines. This indicates that the activity of MnSOD per mitochondrion was increased in the mesothelioma cells. Superoxide production was assayed in the isolated mitochondria of these cells using lucigenin chemiluminescence. Mitochondrial superoxide levels were significantly lower (72%) in the mesothelioma cells compared to the mesothelial cells. Oxidant production in intact cells, assayed by fluorimetry using 2′,7′-dichlorodihydrofluorescein as a fluorescent probe, did not differ significantly between these cells. We conclude that mitochondrial superoxide levels are lower in mesothelioma cells compared to nonmalignant mesothelial cells, and that this difference may be explained by higher MnSOD activity in the mitochondria of these cells. Oxidant production was not different in these cells, which may be due to the previously observed increase in H 2 O 2 -scavenging mechanisms of mesothelioma cells. © 1999 Cancer Research Campaign

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 85%

Section: Mnsod Citrate Synthase and Cytochrome C Oxidasementioning

confidence: 99%

See 1 more Smart Citation

Generation of reactive oxygen species by human mesothelioma cells

et al. 1999

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“…Growing evidence indicates that the antioxidant defence systems of mammalian tissues are capable of adaptation in response to chronic exposure to oxidants. Indeed, it has been shown that exposure of mouse heart to superoxide radicals results in an increased expression of MnSOD (Oberly et al 1987). Following this logic, since prolonged exercise results in an increased production of oxidants in skeletal muscle, chronic exercise training should upregulate muscle antioxidant enzyme activities.…”

Section: Exercise Training and Skeletal Muscle Antioxidant Enzyme Actmentioning

confidence: 99%

Analysis of cellular responses to free radicals: focus on exercise and skeletal muscle

1999

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Muscular exercise results in an increased production of radicals and other forms of reactive oxygen species (ROS). Recent evidence suggests that radicals and other ROS are an underlying aetiology in exercise-induced disturbances in muscle redox status. These exercise-induced redox disturbances in skeletal muscle are postulated to contribute to both muscle fatigue and/or exercise-induced muscle injury. To defend against ROS, muscle cells contain complex cellular defence mechanisms to reduce the risk of oxidative injury. Two major classes (enzymic and non-enzymic) of endogenous protective mechanisms work together to reduce the harmful effects of oxidants in the cell. Primary antioxidant enzymes include superoxide dismutase (EC 1.15.1.1; SOD), GSH peroxidase (EC 1.11.1.9; GPX), and catalase (EC 1.11.1.6); these enzymes are responsible for removing superoxide radicals, H2O2 and organic hydroperoxides, and H2O2 respectively. Important non-enzymic antioxidants include vitamins E and C, β-carotene, GSH and ubiquinones. Vitamin E, β-carotene and ubiquinone are located in lipid regions of the cell, whereas GSH and vitamin C are in aqueous compartments of the cell. Regular endurance training promotes an increase in both total SOD and GPX activity in actively-recruited skeletal muscles. High-intensity exercise training has been shown to be generally superior to low-intensity exercise in the upregulation of muscle SOD and GPX activities. Also, training-induced upregulation of antioxidant enzymes is limited to highly-oxidative skeletal muscles. The effects of endurance training on non-enzymic antioxidants remain a relatively uninvestigated area.

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“…Mn-SOD expression is enhanced by TNF␣ and other inflammatory mediators that cause intracellular release of oxidant compounds. 17,18 Also, other agents and treatments that generate oxidative insult such as x-ray irradiation and hyperoxia 19,20 can induce directly or indirectly the synthesis of Mn-SOD. These observations together with the strategic localization of Mn-SOD in mitochondria, a main site of ROS production, suggest that Mn-SOD is important in the protection against oxidative stress.…”

Section: ⅐ϫmentioning

confidence: 99%

Superoxide Dismutase in Patients With Chronic Hepatitis C Virus Infection

Larrea

Beloqui

Muñoz-Navas

et al. 1998

Free Radical Biology and Medicine

110

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Abstract-It has been reported that hepatitis C virus (HCV) may cause oxidative stress in infected cells. Patients with chronic hepatitis C exhibit an increased production of tumor necrosis factor-␣ (TNF␣), a cytokine that can produce oxidative stress by stimulating the generation of reactive oxygen species (ROS). Cell defense against ROS includes overexpression of Mn-superoxide dismutase (SOD), an inducible mitochondrial enzyme. To investigate cell defense against oxidative stress in HCV infection, we analyzed Mn-SOD mRNA in liver and in peripheral blood mononuclear cells (PBMC) from patients with chronic hepatitis C. Mn-SOD expression in PBMC was significantly increased in patients with HCV infection. Patients with sustained virological and biochemical response after therapy showed significantly lower Mn-SOD than patients with positive viremia. By contrast, Mn-SOD expression was not enhanced in the liver of patients with chronic hepatitis C. The values of Mn-SOD mRNA did not correlate with TNF␣ mRNA expression, viral load, or liver disease activity. Our results indicate that in HCV infection an induction of Mn-SOD was present in PBMC but absent in the liver, suggesting that this organ could be less protected against oxidative damage. Oxidative stress could participate in the pathogenesis of HCV infection.

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Increase in manganese superoxide dismutase activity in the mouse heart after X-irradiation

Cited by 156 publications

References 27 publications

Generation of reactive oxygen species by human mesothelioma cells

Generation of reactive oxygen species by human mesothelioma cells

Analysis of cellular responses to free radicals: focus on exercise and skeletal muscle

Superoxide Dismutase in Patients With Chronic Hepatitis C Virus Infection

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