Nothing in Excess—Lessons Learned from the Expression of High-Mobility Group Proteins Type a in Non-Cancer and Cancer Cells

Petkova, Rumena; Tummala, Hemanth; Zhelev, Nikolai

doi:10.5504/bbeq.2011.0102

Cited by 12 publications

(10 citation statements)

References 42 publications

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“…it has been already demonstrated that the R variant of p53 is associated with higher risk of recurrence of coronary atherosclerotic disease (5). oxidative stress has long been known to be a part of the pathogenetic mechanism in diabetes type 2 and one of the major factors in development of complications (3,40). carriership of the R allele, as a factor predisposing to apoptosis in stressed cells may work towards increasing the risk for accelerated vascular aging in patients with diabetes type 2. the latter is a common complication of diabetes type 2, but does not occur in all patients and is suspected to be closely related to the individual capacity to handle oxidative stress (16,37).…”

Section: Possible Aspects Of Application Of the Mini-panelmentioning

confidence: 99%

Children of the Sun, Children of the Moon—A Mini-Panel for Assessment of Inter-Individual Variation Between the Capacity of Healthy Individuals to Repair Everyday Genotoxic Insults

Chicheva¹,

Chelenkova²,

Petkova³

et al. 2012

Biotechnology & Biotechnological Equipment

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Section: Possible Aspects Of Application Of the Mini-panelmentioning

confidence: 99%

Children of the Sun, Children of the Moon—A Mini-Panel for Assessment of Inter-Individual Variation Between the Capacity of Healthy Individuals to Repair Everyday Genotoxic Insults

Chicheva¹,

Chelenkova²,

Petkova³

et al. 2012

Biotechnology & Biotechnological Equipment

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“…Mutations in human NEIL1 gene are identifiable in 2-3 % of human patients with diabetes type 2 [127]. Insulin resistant diabetes has been suspected as a predisposing factor for cancer [128,129] as well as late-onset dementia [130,131]. The latter may be an effect related to the increased rates of vascular disease in individuals with unmanaged diabetes, but the authors of the cited studies reported decreased rates of clearance of amyloid beta peptide in individuals with high insulin levels.…”

Section: Don't Throw Away Repair It -Capacity To Repair Genotoxic Damentioning

confidence: 99%

APOE4, oxidative stress and decreased repair capacity - a no-brainer. Faulty lipid metabolism and increased levels of oxidative damage may be risk factors in the pathogenesis of late-onset dementia

Nayyar

Chakalova²

2015

Biodiscovery

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Keywords: Late-onset disease, dementia, APOE, mitochondrial DNA, individual repair capacity.Abbreviations: AD -Alzheimer's disease, APOE -apolipoprotein E, ATP -adenosine triphosphate, BER -base excision repair, CAA -cerebral amyloid angiopathy, CNS -central nervous system, FTD -frontotemporal dementia, HD -Huntington's disease, IMT -intimamedia thickness, IRC -individual repair capacity, MCI -mild cognitive impairment, MND -motor neuron disease, NER -nucleotide excision repair, NMDA -N-methyl-D-aspartate, PD -Parkinson's disease, PDAPP -PDGF promoter expressing amyloid precursor protein, ROS -reactive oxygen species; SOD -superoxide dismutase, VCI -vascular cognitive decline.* Corresponding Authors: Ashima Nayyar, email: a.nayyar@abertay.ac.uk Conflict of Interests:No potential conflict of interest was disclosed by any of the authors. AbstractDementia is very common in the elderly and its incidence increases in an age-dependent fashion. Alzheimer's disease and vascular cognitive decline are the most common cases of dementia in the elderly. Amyloid burden and increased levels of oxidative damage have been implicated to play significant roles in the pathogenesis of late-onset dementia. In this paper we propose that there are three major genetic factors that may modulate the risk for dementia in later life: carriership of APOE variant alleles, carriership of mitochondrial DNA of haplogroups associated with ineffective oxygen utilisation (specifically, haplogroup H) and carriership of genetic polymorphisms conferring subtly deficient DNA repair. All three factors are quite common in the European populations. Each of these three factors may not have significant effect on the phenotype when taken separately, but when combined in the same genotype, the effects may be cumulative. Further studies are needed in order to elucidate the genotype-phenotype relationships and provide a reliable basis for assessment of the genetic risk for sporadic late-onset dementia. Lifestyle alterations and therapies targeted at decreasing the oxidative burden to aging cells and tissues may decrease the risk for neurological decline in later life.

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“…Abnormal placentation and subsequent vascular dysfunction are common in women that later develop gestational diabetes. Poorly managed oxidative stress is known to be a major factor in the pathogenesis of insulin resistance and its associated complications [117][118][119]. Nevertheless, very few studies have been published with regard to the association of the maternal level of oxidative damage in and gestational diabetes, all of these in the last 5 years.…”

Section: Role Of the Individual Repair Capacity In The Constitution Omentioning

confidence: 99%

Reproductive outcomes in pregnant women aged 35 or older: the role of individual repair capacity

Petkova¹,

Dimitrova²,

Zhelev³

et al. 2015

Biodiscovery

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Abbreviations: 8-OH-dG -8-hydroxydeoxyguanosine, AMA -advanced maternal age, AR -assisted reproduction, BER -base excision repair, CDC -US Centre for disease prevention and control, DIC -disseminated intravascular coagulation, DS -Down syndrome, HELLP -haemolysis/elevated liver enzymes/low platelets, ICSI -intracytoplasmic sperm injection, IRC -individual repair capacity, IUGR -intrauterine growth restriction, IUI -intrauterine insemination, IVF -in vitro fertilisation, LIF -leukaemia inhibitory factor, NER -nucleotide excision repair, PCOS -polycystic ovary syndrome, PIH -pregnancy-induced hypertension, ROS -reactive oxygen species, TTD -trichothiodystrophy, w.g. -weeks of gestation, WHO -World Health Organisation, XP -xeroderma pigmentosum. AbstractAt present, childbirth is being progressively postponed until later age. Women aged 35 or older may have to wait longer to conceive than younger women and are more likely to be referred to fertility evaluations, but in a significant proportion a spontaneous conception would be achieved in the timeframe typical of younger women. Pregnancies where mothers are ≥ 35 are associated with more risks for pregnancy loss, chromosomal disease, pregnancy-associated complications, prematurity and low birthweight. These concerns, however, are not uncommon in younger women as well. This puts forward the question whether advanced age per se is the underlying cause for the increased risk for adverse outcomes in older pregnant women, or whether there might be other factors that account for it but do not radically worsen the prospects for favourable outcomes. The individual risks associated with childbirth late in life may stem from maternal genetic background rather than being a simple function of age. There is plenty of preliminary evidence that individual capacity for identification and repair of DNA damage may constitute a major factor in female fertility and fecundity. Subtle deficiencies in the repair capacity may have little to no importance in younger pregnant women but may make a significant difference in older women. The outcomes of pregnancies in women >35 are largely dependent on the prepregnancy health status and the quality of antenatal care, and may not be dramatically different from outcomes in younger women.

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Nothing in Excess—Lessons Learned from the Expression of High-Mobility Group Proteins Type a in Non-Cancer and Cancer Cells

Cited by 12 publications

References 42 publications

Children of the Sun, Children of the Moon—A Mini-Panel for Assessment of Inter-Individual Variation Between the Capacity of Healthy Individuals to Repair Everyday Genotoxic Insults

Children of the Sun, Children of the Moon—A Mini-Panel for Assessment of Inter-Individual Variation Between the Capacity of Healthy Individuals to Repair Everyday Genotoxic Insults

APOE4, oxidative stress and decreased repair capacity - a no-brainer. Faulty lipid metabolism and increased levels of oxidative damage may be risk factors in the pathogenesis of late-onset dementia

Reproductive outcomes in pregnant women aged 35 or older: the role of individual repair capacity

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