Lipid Peroxidation, Superoxide Dismutase and Catalase Activities in Brain Tumor Tissues

Popov, B.; Gadjeva, V.; Valkanov, P.; Popova, S.; Toleкova, A.

doi:10.3109/13813450312331342328

Cited by 40 publications

(27 citation statements)

References 22 publications

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“…SOD is an enzyme that catalyzes the dismutation of the superoxide radical (O 2 ·− ) very efficiently ( k 2 ~2 × 10 9 M −1 s −1 ) through a redox reaction of its copper centre enzyme into oxygen (O 2 ) and hydrogen peroxide (H 2 O 2 ). Today, it is clear that decrease of enzymatic activity of the defense system or an overwhelming production of O 2 ·− and/or H 2 O 2 is linked to neurodegenerative disorders (e.g., familial amyotrophic lateral sclerosis [12], AD [13], PD [14], and cancer [15]). The idea that oxygen might not only be involved in the beginning of life and evolution [16–18] but also it might be a toxic molecule [19] was further popularized by Halliwell and Gutteridge in their book entitled “Free Radicals in Biology and Medicine” [20] and some important follow-up papers [21–23].…”

Section: The Verdict: Oxygen Is Guilty Not Guiltymentioning

confidence: 99%

The Bad, the Good, and the Ugly about Oxidative Stress

Jiménez-Del-Río

Vélez-Pardo

2012

Oxidative Medicine and Cellular Longevity

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Alzheimer's disease (AD), Parkinson's disease (PD), and cancer (e.g., leukemia) are the most devastating disorders affecting millions of people worldwide. Except for some kind of cancers, no effective and/or definitive therapeutic treatment aimed to reduce or to retard the clinic and pathologic symptoms induced by AD and PD is presently available. Therefore, it is urgently needed to understand the molecular basis of these disorders. Since oxidative stress (OS) is an important etiologic factor of the pathologic process of AD, PD, and cancer, understanding how intracellular signaling pathways respond to OS will have a significant implication in the therapy of these diseases. Here, we propose a model of minimal completeness of cell death signaling induced by OS as a mechanistic explanation of neuronal and cancer cell demise. This mechanism might provide the basis for therapeutic design strategies. Finally, we will attempt to associate PD, cancer, and OS. This paper critically analyzes the evidence that support the “oxidative stress model” in neurodegeneration and cancer.

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Section: The Verdict: Oxygen Is Guilty Not Guiltymentioning

confidence: 99%

The Bad, the Good, and the Ugly about Oxidative Stress

Jiménez-Del-Río

Vélez-Pardo

2012

Oxidative Medicine and Cellular Longevity

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“…Oxidative stress might occur in the background of alteration in optimum levels of trace elements leading to metabolic disorders and changes in cellular structure. Exposure to reactive oxygen species (ROS) can lead to direct DNA damage, mutation, and carcinogenesis [6,7]. Previous studies have reported alterations in the concentrations of serum or neoplastic tissue trace elements in various carcinomas including breast, bladder, gastric, gallbladder, and lung cancers [1,[8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Serum Copper and Zinc Levels Among Iranian Colorectal Cancer Patients

Khoshdel

Naghibalhossaini

Abdollahi

et al. 2015

Biol Trace Elem Res

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Alterations of trace element concentrations adversely affect biological processes and could promote carcinogenesis. Only a few studies have investigated the degree of changes in copper and zinc levels in colorectal cancer (CRC). The aim of the present study was to compare the serum copper (Cu) and zinc (Zn) concentrations in patients with CRC from Iran with those of healthy subjects. Cu and Zn concentrations in the serum of 119 cancer patients and 128 healthy individuals were measured by atomic absorption spectrometry. We found a significant decrease in the total mean serum Cu and Zn concentrations in CRC patients as compared with the control group (137.5 ± 122.38 vs. 160.68 ± 45.12 μg/dl and 81.04 ± 52.05 vs. 141.64 ± 51.75, respectively). However, the serum Cu/Zn ratio in the patient group was significantly higher than that measured in the control group (p = 0.00). There was no significant difference in the mean values of serum Cu and Zn concentrations between young (<60 years) and elderly (≥60 years) patients. However, the Cu/Zn ratio in <60-year cases was significantly higher than that in ≥60-year age group (p < 0.05). In addition, mean serum Cu level in normal weight patients was significantly higher than that in overweight/obese cases (132.31 ± 87.43 vs. 103.81 ± 53.72 μg/dl, respectively) (p < 0.05). There was no difference in mean serum Cu and Zn concentrations in patients stratified by the site, stage, or differentiation grade of tumors. Our findings suggest that imbalance in Cu and Zn trace element level is associated with CRC and might play an important role in cancer development among Iranian patients.

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“…Chronic hyperglycemia-induced oxidative stress is considered the most important factor in TGF-β1 production, which can lead to renal injury and interstitial fibrosis (Forbes et al, 2008). MDA is the end-product of lipid peroxidation and is considered as a marker of oxidative stress (Popov et al, 2003). Our data showed that the production of ROS and MDA were increased in the DM-induced diabetic group, which was accompanied by the impairment of SOD activity, while lovastatin considerably reduced the generation of ROS and MDA, and also it up-regulated the activity of SOD, in addition, lovastatin decreased the expression of NOX4 in the DM-induced diabetic group.…”

Section: Discussionmentioning

confidence: 99%

Lovastatin Alleviates Endothelial-to-Mesenchymal Transition in Glomeruli via Suppression of Oxidative Stress and TGF-β1 Signaling

Zhu

Liu

et al. 2017

Front. Pharmacol.

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Statins may decrease chronic kidney diseases (CKDs) risk, but their underlying molecular mechanisms are not completely understood. Recent studies indicate Endothelial-to-mesenchymal transition (EndMT) plays an important role contributing to renal interstitial fibrosis. In the present study, we first investigated whether lovastatin could ameliorate renal fibrosis via suppression of EndMT and its possible mechanism. In vitro experiments, lovastatin significantly ameliorated microalbuminuria and pathologic changes in diabetic rats. Double labeling immunofluorescence showed lovastatin could inhibit EndMT in glomeruli. Furthermore, lovastatin could inhibit oxidative stress and down-regulate TGF-β1-Smad signaling. Consistent alterations were observed in vivo that lovastatin substantially suppressed EndMT and TGF-β1 signaling induced by high glucose in glomerular endothelial cells (GEnCs). These data indicated that lovastatin could ameliorate EndMT in glomeruli in diabetic nephropathy, the mechanism of which might be at least partly through suppression of oxidative stress and TGF-β1/Smad signaling pathway.

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Lipid Peroxidation, Superoxide Dismutase and Catalase Activities in Brain Tumor Tissues

Cited by 40 publications

References 22 publications

The Bad, the Good, and the Ugly about Oxidative Stress

The Bad, the Good, and the Ugly about Oxidative Stress

Serum Copper and Zinc Levels Among Iranian Colorectal Cancer Patients

Lovastatin Alleviates Endothelial-to-Mesenchymal Transition in Glomeruli via Suppression of Oxidative Stress and TGF-β1 Signaling

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