Hydrogen peroxide and sequence‐specific DNA damage in human cells

Burdon, Roy H.; Gill, Vera; Boyd, Patricia A.; Rahim, Raha Abdul

doi:10.1016/0014-5793(96)00230-x

Cited by 14 publications

(8 citation statements)

References 24 publications

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“…In addition to being generated during cellular metabolism in mitochondria, ROS can be produced in response to different environmental stimuli such as growth factors, inflammatory cytokines, chemical oxidants and chemotherapeutics. Dependent on cell types ROS have been found to function as signaling molecules in cell proliferation and cellular senescence [47], or cell death [48]. The observation of increased autophagy in the brains of patients with AD, PD and HD suggests that autophagy contributes to the pathogenesis of these neurodegenerative diseases; a possible cause is increased cell death [49] because of the constant production of free radicals in mitochondria and changes in the antioxidant system which leads to imbalance, oxidative stress, and neurodegeneration [40].…”

Section: Mitochondria and Redox Stressmentioning

confidence: 99%

Autophagy of Mitochondria: A Promising Therapeutic Target for Neurodegenerative Disease

Kamat

Kalani

Kyles

et al. 2014

Cell Biochem Biophys

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The autophagic process is the only known mechanism for mitochondrial turnover and it has been speculated that dysfunction of autophagy may result in mitochondrial error and cellular stress. Emerging investigations have provided new understanding of how autophagy of mitochondria (also known as mitophagy) is associated with cellular oxidative stress and its impact on neuro-degeneration. This impaired autophagic function may be considered as a possible mechanism in the pathogenesis of several neurodegenerative disorders including: Parkinson's disease (PD), Alzheimer's disease (AD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS) and Huntington disease (HD). It can be suggested that autophagy dysfunction along with oxidative stress are considered main events in neurodegenerative disorders. New therapeutic approaches have now begun to target mitochondria as a potential drug target. This review discusses evidence supporting the notion that oxidative stress and autophagy are intimately associated with neurodegenerative disease pathogenesis. This review also explores new approaches that can prevent mitochondrial dysfunction, improve neurodegenerative etiology, and also offer possible cures to the aforementioned neurodegenerative diseases.

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Section: Mitochondria and Redox Stressmentioning

confidence: 99%

Autophagy of Mitochondria: A Promising Therapeutic Target for Neurodegenerative Disease

Kamat

Kalani

Kyles

et al. 2014

Cell Biochem Biophys

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“…Although the sample size of SIDS DNAs used was small it was sufficiently large to detect frequent polymorphisms.5 Importantly, no novel RFLP was detected in the DNAs from infants dying from SIDS. Although no new fragments were revealed, the 6 (table 1). Polymorphisms associated with hsp7O have been reported previously.4 With regard to SIDS, however, the apparent significant association with a polymorphism in the gene encoding hsp60 is novel and of potential importance.…”

mentioning

confidence: 96%

“…In terms of a potential cause it may be relevant that other studies have shown that the loss of the hsp60 15.0 kb MspI fragment also occurs in human cells exposed in vitro to the endogenous oxidant hydrogen peroxide. 6 In terms of function hsp60 itself appears to have an important role in mitochondrial biogenesis,' and impaired mitochondrial function could be a contributory factor in SIDS. Indeed, possible mitochondrial dysfunction in infants dying from SIDS has been observed in the shape of inappropriate brown adipose tissue thermogenesis.7 This alteration of frequency of a polymorphic fragment between SIDS and control DNAs may in the future provide the basis of a test to indicate a predisposition to SIDS, the occurrence of which could be limited by good paediatric care.…”

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confidence: 99%

Human heat shock protein gene polymorphisms and sudden infant death syndrome.

Rahim

Boyd

Patrick

et al. 1996

Archives of Disease in Childhood

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Comparison of the frequency of occurrence of restriction fragment length polymorphisms in control human DNAs and DNAs from infants dying from sudden infant death syndrome has indicated no significant difference in the case of restriction fragment length polymorphisms associated with the heat shock protein genes hsp7O and hsp9O. A highly significant difference was detected, however, in the case of the specific restriction fragment length polymorphisms detected by an hsp6O gene probe in MspI digests. (Arch Dis Child 1996;75:451-452) Keywords: heat shock proteins, restriction fragment length polymorphisms, sudden infant death syndrome, heat shock protein 60.Heat shock proteins play a central part in the normal physiology of cells.' Although they appear to be involved in the acquisition and maintenance of thermotolerance, other major roles include the repair of denatured cell proteins and functions as molecular 'chaperones' in the intracellular transmembrane transport of cellular proteins and in the construction of complex quaternary cellular protein structures. At present the cause of sudden infant death syndrome (SIDS) is unclear. Some deaths have been attributed to fever-like disorders,2 possibly brought on by overwrapping or by a virus infection. A possibility is that infants are susceptible to SIDS because some of the heat shock proteins are not produced or are defective, thus providing inadequate thermal protection. This could arise from defects in the DNA associated with genes encoding critical heat shock proteins. Results and discussion An initial screen of healthy human subjects was undertaken to determine whether sequence probes to the heat shock protein genes, hsp6O, hsp7O, and hsp9O could reveal any restriction fragment length polymorphisms (RFLPs). A panel of 26 genomic DNA samples was digested with 19 different restriction enzymes to detect RFLPs. Use of the hsp7o probe detected variations in these control samples digested with BgII, PstI and PvuII, as previously reported by Goate et al. 4 The DNAs digested with MspI or ScaI were also polymorphic for hsp6O, and the hsp90 probe detected variations in samples digested with Sau961. The frequency of the variable fragments was determined for all polymorphisms (table 1). The RFLPs detected using the hsp60 probe were more complex than those found using the hsp7O probe. With MspI, 16 constant fragments and six variant fragments were detected in 26 individuals. There was one hsp9o associated polymorphism, detected with Sau961 digested DNA. Nine of the fragments were invariant, whereas two others displayed a polymorphism characteristic of a two allele system.To determine if there was any difference in the nature of heat shock protein gene polymorphisms in infants dying from SIDS compared with the controls, 12 DNA samples from SIDS infants were examined with the same 19 restriction enzymes used in the initial screening for heat shock protein polymorphisms. Although the sample size of SIDS DNAs used was small it was sufficiently large to detect frequent...

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“…1993; Dukan and Touati 1996). In cells, ROS can exert either beneficial effects by mediating several physiological processes (Burdon et al. 1996; Finkel and Holbrook 2000; Tomankova et al.…”

Section: Introductionmentioning

confidence: 99%

Cellular damage induced by a sequential oxidative treatment on Penicillium digitatum

Cerioni

Volentini

Prado

et al. 2010

Journal of Applied Microbiology

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Aim: To investigate the cellular damage on Penicillium digitatum produced by a sequential oxidative treatment (SOT), previously standardized in our laboratory, to prevent the conidia growth. Lethal SOT consists of 2‐min preincubation with 10 ppm NaClO followed by 2‐min incubation with 6 mmol l−1 CuSO4 and 100 mmol l−1 H2O2 at 25°C. Methods and Results: After the application of lethal SOT or sublethal SOT (decreasing only the H2O2 concentration), we analysed several conidia features such as germination, oxygen consumption, ultrastructure and integrity of the cellular wall and membrane. Also, we measured the production of reactive oxygen species (ROS) and the content of thiobarbituric acid‐reactive species (TBARS). With the increase of H2O2 concentration in the SOT, germination and oxygen consumption of conidia became inhibited, while the membrane permeability, ROS production and TBARS content of conidia increased. Several studies revealed ultrastructural disorganization in P. digitatum conidia after lethal SOT, showing severe cellular damage without apparent damage to the cell wall. In addition, mycelium of P. digitatum was more sensitive than conidia to the oxidative treatment, because growth ceased and permeability of the membranes increased after exposure of the mycelium to a SOT with only 50 mmol l−1 H2O2 compared to a SOT of 100 mmol l−1 for these effects to occur on conidia. Conclusion: Our insights into cellular changes produced by the lethal SOT are consistent with the mode of action of the oxidant compounds, by producing both alteration of membrane integrity and intracellular damage. Significance and Impact of the Study: Our results allow the understanding of SOT effects on P. digitatum, which will be useful to develop a reliable treatment to control postharvest diseases in view of its future application in packing houses.

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Hydrogen peroxide and sequence‐specific DNA damage in human cells

Cited by 14 publications

References 24 publications

Autophagy of Mitochondria: A Promising Therapeutic Target for Neurodegenerative Disease

Autophagy of Mitochondria: A Promising Therapeutic Target for Neurodegenerative Disease

Human heat shock protein gene polymorphisms and sudden infant death syndrome.

Cellular damage induced by a sequential oxidative treatment on Penicillium digitatum

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