1,721,042 research outputs found
Commenting on Gorpinchenko et al. The influence of direct mobile phone radiation on sperm quality
No full textEditorial: Sirtuinome Rewiring to Hijack Cancer Cell Behavior and Hamper Resistance to Anticancer Intervention
Full text linkIn this Research Topic we collected original studies (mini)review and perspective articles that were focused on the SIRT-dependent mechanisms that underlie various tumor- and cancer-related processes, both at cellular and tissue level
Editorial: Extracellular vesicles as modulators of cancer cell adaptive responses linked to therapy resistance
No full textRNA methylation and cellular response to oxidative stress-promoting anticancer agents
No full textDisruption of the complex network that regulates redox homeostasis often underlies resistant phenotypes, which hinder effective and long-lasting cancer eradication. In addition, the RNA methylome-dependent control of gene expression also critically affects traits of cellular resistance to anti-cancer agents. However, few investigations aimed at establishing whether the epitran- scriptome-directed adaptations underlying acquired and/or innate resistance traits in cancer could be implemented through the involvement of redox-dependent or -responsive signaling pathways. This is unexpected mainly because: i) the effectiveness of many anti-cancer approaches relies on their capacity to promote oxidative stress (OS); ii) altered redox milieu and reprogramming of mitochondrial function have been acknowledged as critical mediators of the RNA methylome- mediated response to OS. Here we summarize the current state of understanding on this topic, as well as we offer new perspectives that might lead to original approaches and strategies to delay or prevent the problem of refractory cancer and tumor recurrence
Osteoblast-derived extracellular vesicles influence MNNG/HOS osteosarcoma cells, reducing their migration and affecting their metabolic activity and redox balance
No full textOxidative stress and reprogramming of mitochondrial function and dynamics as targets to modulate cancer cell behavior and chemoresistance
Full text linkSirt1 is essential for beneficial effect of resveratrol on HG-induced endothelial dysfunction
Full text linkHigh levels of antioxidant enzymatic defence assure good protection against hypoxic stress in spontaneously diabetic rats
No full textRecent data from literature report that reactive oxygen species (ROS) seem to play a crucial role in the etiology of both types
I and II diabetes. This may render diabetic individuals more prone to oxidative injury when challenged with hypoxic stress. It is
in fact well known that many diabetic complications cause ischaemic episodes, with a consequent reduction in oxygen supply to
various tissues and organs.
To check this hypothesis, in this work we tested type I diabetic individuals’ antioxidant capability towards a hypoxic-mediated
oxidative challenge. In particular, spontaneously diabetic and age-matched non-diabetic biobreeding (BB)Wistar rats were submitted
to chronic normobaric hypoxia, and the response of antioxidant enzymes, as well as redox-sensitive transcription factor NF-B and
p53, were monitored.
Results show that diabetic subjects present a dramatic enhancement in the major antioxidant enzymes activities, thus supporting
the notion of diabetes-related changes in cellular redox status. This allows diabetic individuals to counteract hypoxia-mediated
oxidative challenge better than the non-diabetic counterpart.
Also the behaviour of both the redox-sensitive nuclear transcription factor NF-B and p53 protein in response to hypoxic
stimulation seems to support the hypothesis of a better ROS scavenging efficiency in diabetics under hypoxic conditions.
In conclusion, high levels of antioxidant enzymatic defences in diabetic BB rats reflect a positive adaptive response able to assure
an efficient protection not only against chronic, diabetes-mediated reactive oxygen species (ROS) overproduction, but also versus
further oxidative damage.
© 2006 Elsevier Ltd. All rights reserved
Altered inflammasome machinery as a key player in the perpetuation of Rett syndrome oxinflammation
Full text linkRett syndrome (RTT) is a progressive neurodevelopmental disorder mainly caused by mutations in the X-linked MECP2 gene. RTT patients show multisystem disturbances associated with an oxinflammatory status. Inflammasomes are multi-protein complexes, responsible for host immune responses against pathogen infections and redox-related cellular stress. Assembly of NLRP3/ASC inflammasome triggers pro-caspase-1 activation, thus, resulting in IL-1β and IL-18 maturation. However, an aberrant activation of inflammasome system has been implicated in several human diseases. Our aim was to investigate the possible role of inflammasome in the chronic subclinical inflammatory condition typical of RTT, by analyzing this complex in basal and lipopolysaccharide (LPS)+ATP-stimulated primary fibroblasts, as well as in serum from RTT patients and healthy volunteers. RTT cells showed increased levels of nuclear p65 and ASC proteins, pro-IL-1β mRNA, and NLRP3/ASC interaction in basal condition, without any further response upon the LPS + ATP stimuli. Moreover, augmented levels of circulating ASC and IL-18 proteins were found in serum of RTT patients, which are likely able to amplify the inflammatory response. Taken together, our findings suggest that RTT patients exhibited a challenged inflammasome machinery at cellular and systemic level, which may contribute to the subclinical inflammatory state feedback observed in this pathology
Late-onset running biphasically improves redox balance, energy- and methylglyoxal-related status, as well as SIRT1 expression in mouse hippocampus
No full text"Despite the active research in this field, molecular mechanisms underlying exercise- induced beneficial effects on brain physiology and functions are still matter of debate, especially with regard to biological processes activated by regular exercise affecting the onset and progression of hippocampal aging in individuals unfamiliar with habitual physical activity. Since such responses seem to be mediated by changes in antioxidative, antiglycative and metabolic status, a possible exercise-induced coordinated response involving redox, methylglyoxal- and sirtuin-related molecular networks may be hypothesized.. In this study, hippocampi of CD1 mice undergoing the transition from mature to middle age were analyzed for redox-related profile, oxidative and methylglyoxal-dependent damage patterns, energy metabolism, sirtuin1 and glyoxalase1 expression after a 2- or 4-mo treadmill running program. Our findings suggested that the 4-mo regular running lowered the chance of dicarbonyl and oxidative stress, activated mitochondrial catabolism and preserved sirtuin1-related neuroprotection. Surprisingly, the same cellular pathways were negatively affected by the first 2 months of exercise, thus showing an interesting biphasic response.. In conclusion, the duration of exercise caused a profound shift in the response to regular running within the rodent hippocampus in a time-dependent fashion. This research revealed important details of the interaction between exercise and mammal hippocampus during the transition from mature to middle age, and this might help to develop non-pharmacological approaches aimed at retarding brain senescence, even in individuals unfamiliar with habitual exercise.
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