Superoxide dismutases and their impact upon human health

Johnson, Felicity; Giulivi, Cecilia R

doi:10.1016/j.mam.2005.07.006

Cited by 389 publications

(288 citation statements)

References 56 publications

(54 reference statements)

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“…Also, our results show that lipocalin-2 induces SOD 1, 2 . This is in line with the observation that enhancement of transcription of SOD genes is a part of cellular stress response (Mruk et al 2002, Hartog et al 2003, Johnson and Giulivi 2005, Liochev and Fridovich 2007 and it has been shown that such stressful conditions up-regulate both lipocalin-2 and SOD genes (Lavrovsky et al 1994, Immenschuh and Ramadori 2000, Lavrovsky et al 2000, Zelko et al 2002, Rivera et al 2006, Limón-Pacheco and Gonsebatt 2009. Therefore, our data can indicate that lipocalin-2 by induction of SOD gene adds to the cellular ability to counteract the oxidant challenge.…”

Section: Discussionsupporting

confidence: 91%

Neutrophil Gelatinase-Associated Lipocalin induces the expression of heme oxygenase-1 and superoxide dismutase 1, 2

Bahmani

Halabian

Rouhbakhsh

et al. 2010

Cell Stress and Chaperones

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Lipocalin-2 (Lcn2, NGAL) is a member of the lipocalin super family with diverse function such as the induction of apoptosis, the suppression of bacterial growth, and modulation of inflammatory response. Much interest has recently been focused on the physiological/pathological role of the lipocalin-2 that is considered to be a novel protective factor against oxidative stress. However, its precise biological roles in this protection are not fully understood. In this report we intended to test the effect of lipocalin-2 on the expression of heme oxygenase (1, 2) and superoxide dismutase (1, 2) which are two strong antioxidants. NGAL was cloned to pcDNA3.1 plasmid by using genetic engineering method. The recombinant vector was transfected to CHO and HEK293T to establish stable cell expressing NGAL and the expression of HO-1, 2 and SOD 1, 2 were compared with appropriate controls by RT-PCR and western blot. On the other hand, expression of NGAL was suppressed by siRNA transfection in order to study the effect of lipocalin-2 on mentioned genes/proteins. The results showed that the expression of HO-1 and SOD 1, 2 enzymes were higher in cells expressing recombinant lipocalin-2 compared with the control cells. Although the expression of HO-1 was lower in NGAL silencing cells, the expression of SOD 1 and SOD 2 were higher. Our data suggest that NGAL is a potent inducer of HO-1 and somewhat SOD 1 and SOD 2 and it appears that part of antioxidant property of NGAL could be attributed to the induction of HO-1and SOD 1, 2 .

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Section: Discussionsupporting

confidence: 91%

Neutrophil Gelatinase-Associated Lipocalin induces the expression of heme oxygenase-1 and superoxide dismutase 1, 2

Bahmani

Halabian

Rouhbakhsh

et al. 2010

Cell Stress and Chaperones

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“…BA's protective role derives from its stimulatory effect on SOD, CAT, GSH-Px and GSH and its inhibitory action on MDA. SOD catalyses the dismutation of superoxide to hydrogen peroxide and oxygen which are deleterious to polyunsaturated fatty acids and structural proteins of plasma membrane (Johnson and Giulivi 2005). Endogenous H 2 O 2 is converted to H 2 O by catalase (Svistunenko 2005).…”

Section: Discussionmentioning

confidence: 99%

Boric acid: a potential chemoprotective agent against aflatoxin b1 toxicity in human blood

Türkez

Geyikoğlu

2010

Cytotechnology

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Aflatoxin B 1 is the most potent pulmonary and hepatic carcinogen. Since the eradication of Aflatoxin B 1 contamination in agricultural products has been difficult, the use of natural or synthetic free radical scavengers could be a potential chemopreventive strategy. Boric acid is the major component of industry and its antioxidant role has recently been reported. The present study assessed, for the first time, the effectiveness of boric acid following exposure to Aflatoxin B 1 on human whole blood cultures. The biochemical characterizations of glutathione and some enzymes have been carried out in erythrocytes. Alterations in malondialdehyde level were determined as an index of oxidative stress. The sister-chromatid exchange and micronucleus tests were performed to assess DNA damages in lymphocytes. Aflatoxin B 1 treatment significantly reduced the activities of antioxidants by increasing malondialdehyde level (30.53 and 51.43%) of blood, whereas, the boric acid led to an increased resistance of DNA to oxidative damage induced by Aflatoxin B 1 in comparison with control values (P \ 0.05). In conclusion, the support of boric acid was especially useful in Aflatoxin-toxicated blood. Thus the risk on tissue targeting of Aflatoxin B 1 could be reduced ensuring early recovery from its toxicity.

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“…SOD competes with nitric oxide for reaction with superoxide and prevents generation of peroxynitrite, a potent oxidant that can modify proteins to form 3-nitrotyrosine. 33 Thus, sufficient amounts of catalytically competent SOD are required to prevent tissue damage. SOD is a target of tyrosine nitration and nitration inactivates the enzyme.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of aminoguanidine against oxidative stress and bladder injury in cyclophosphamide‐induced hemorrhagic cystitis in rat

Abraham

Rabi

Selvakumar

2008

Cell Biochemistry & Function

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Cyclophosphamide (CP) is an antineoplastic agent that is used for the treatment of many neoplastic diseases. Hemorrhagic cystitis (HC) is a major dose limiting side effect of CP. Recent studies show that aminogaunidine, an inhibitor of inducible nitric oxide synthase is a potent antioxidant and prevents changes caused by oxidative stress such as depletion of antioxidant activity and tissue injury. The purpose of the study is to investigate the effect of aminoguanidine on parameters of oxidative stress, antioxidant enzymes and bladder injury caused by CP. Adult male rats were randomly divided into four groups. Control rats were administered saline; the AG control group received 200 mg/kg body wt of aminoguanidine; The CP group received a single injection of CP at the dose of 150 mg/kg body wt intraperitoneally. The CP þAG group received aminoguanidine (200 mg/kg body wt) intraperitoneally 1 h before the administration of CP. The rats were sacrificed 16 h after CP/saline administration. The bladder was used for light microscopic studies and biochemical studies. The markers of oxidative damage including protein carbonyl content, protein thiol, malondialdehyde and conjugated dienes were assayed in the homogenates along with the activities of the antioxidant enzymes, superoxide dismutase, glutathione peroxidase, catalase, and glutathione reductase and glutathione S transferase. In the bladders of CP treated rats edema of lamina propria with epithelial and sub-epithelial hemorrhage was seen. All the parameters of oxidative stress that were studied were significantly elevated in the bladders of CP treated rats. The activities of the antioxidant enzymes were significantly lowered in the bladders of CP treated rats. Aminoguanidine pretreatment prevented CP-induced oxidative stress, decrease in the activities of anti-oxidant enzymes and reduced bladder damage. The results of the present study suggest the antioxidant role for aminoguanidine in CP-induced bladder damage.

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Superoxide dismutases and their impact upon human health

Cited by 389 publications

References 56 publications

Neutrophil Gelatinase-Associated Lipocalin induces the expression of heme oxygenase-1 and superoxide dismutase 1, 2

Neutrophil Gelatinase-Associated Lipocalin induces the expression of heme oxygenase-1 and superoxide dismutase 1, 2

Boric acid: a potential chemoprotective agent against aflatoxin b1 toxicity in human blood

Protective effect of aminoguanidine against oxidative stress and bladder injury in cyclophosphamide‐induced hemorrhagic cystitis in rat

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