Oxidative Stress Profiling:

Cutler, Richard G.

doi:10.1196/annals.1323.027

Cited by 65 publications

(43 citation statements)

References 115 publications

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“…A life-time accumulation of sublethal oxidative stress damage through open gap junctions would be harmful. Oxidative stress is one of the most common causative agents of disease (Cutler, 2005). Prolonged oxidative stress (such as long term H 2 O 2 treatment for 24·h) causes protein oxidation, aggregation, degeneration and cell death.…”

Section: Discussionmentioning

confidence: 99%

PKCγ knockout mouse lenses are more susceptible to oxidative stress damage

Lin

Barnett

Lobell

et al. 2006

Journal of Experimental Biology

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SUMMARY Cataracts, or lens opacities, are the leading cause of blindness worldwide. Cataracts increase with age and environmental insults, e.g. oxidative stress. Lens homeostasis depends on functional gap junctions. Knockout or missense mutations of lens gap junction proteins, Cx46 or Cx50, result in cataractogenesis in mice. We have previously demonstrated that protein kinase Cγ (PKCγ) regulates gap junctions in the lens epithelium and cortex. In the current study, we further determined whether PKCγ control of gap junctions protects the lens from cataractogenesis induced by oxidative stress in vitro, using PKCγ knockout and control mice as our models. The results demonstrate that PKCγ knockout lenses are normal at 2 days post-natal when compared to control. However, cell damage, but not obvious cataract, was observed in the lenses of 6-week-old PKCγ knockout mice,suggesting that the deletion of PKCγ causes lenses to be more susceptible to damage. Furthermore, in vitro incubation or lens oxidative stress treatment by H2O2 significantly induced lens opacification (cataract) in the PKCγ knockout mice when compared to controls. Biochemical and structural results also demonstrated that H2O2 activation of endogenous PKCγ resulted in phosphorylation of Cx50 and subsequent inhibition of gap junctions in the lenses of control mice, but not in the knockout. Deletion of PKCγaltered the arrangement of gap junctions on the cortical fiber cell surface,and completely abolished the inhibitory effect of H2O2on lens gap junctions. Data suggest that activation of PKCγ is an important mechanism regulating the closure of the communicating pathway mediated by gap junction channels in lens fiber cells. The absence of this regulatory mechanism in the PKCγ knockout mice may cause those lenses to have increased susceptibility to oxidative damage.

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Section: Discussionmentioning

confidence: 99%

PKCγ knockout mouse lenses are more susceptible to oxidative stress damage

Lin

Barnett

Lobell

et al. 2006

Journal of Experimental Biology

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“…RRR-α-5-(C 2 H 3 ) tocopheryl acetate and all rac-α-5,7-(C 2 H 3 ) 2 tocopheryl acetate (d 3 -RRR-α-α-tocopheryl acetates and d 6 -all rac-α-tocopheryl acetates, respectively) were a gift from the Natural Source Vitamin E Association (NSVEA). The compounds were determined to be 96% RRR-α-tocopheryl acetate and 93% all rac-α-tocopheryl acetate by weight.…”

Section: Deuterated Vitamin Ementioning

confidence: 99%

Burn and smoke inhalation injury in sheep depletes vitamin E: Kinetic studies using deuterated tocopherols

Traber

Shimoda

Murakami

et al. 2007

Free Radical Biology and Medicine

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To test the hypothesis that burn and smoke injury will deplete tissue α-tocopherol and cause its faster plasma disappearance, deuterium-labeled vitamin E was administered to sheep exposed to both surface skin burn and smoke insufflation that causes injury similar to human victims of fire accidents. Two different protocols were used: 1) deuterated vitamin E was administered orally with food at 0 time (just prior to injury), or 2) the labeled vitamin E was administered orally with food the day prior to injury. The animals that had been operatively prepared seven days before, were anaesthetized, then received both 40% body surface area 3rd° burn and 48 breaths of cotton smoke, or sham injuries. All were resuscitated with Ringer's lactate solution (4 ml/kg/% BSA burn/24h) and mechanically ventilated. Blood samples were collected at various times after vitamin E dosing. In both studies the depletion of plasma α-tocopherol was faster in the injured sheep. The sheep given deuterated vitamin E 24 h prior to injury had similar maximum α-tocopherol concentrations at similar times. The exponential rates of α -tocopherol disappearance were 1.5 times greater and half-lives were 12 h shorter (p<0.05) in the injured sheep. In separate studies, various tissues were obtained from sheep that were sacrificed from 4 h to 48 h after injury. The liver α -tocopherol concentrations in sheep killed at various times after injury appear to show a linear decrease at a rate of 0.1 nmol α -tocopherol/ g liver per hour, suggesting that the liver is supplying α -tocopherol to maintain the plasma and lung α -tocopherol concentrations, but that this injury is so severe that the liver is unable to maintain lung α -tocopherol concentrations. These findings suggest that α -tocopherol should be administered to burn patients to prevent vitamin E depletion and to protect against oxidative stress from burn injury.

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“…While evidence is mounting that control of such oxidative processes is essential to curb detrimental conditions, 6 compounds that efficiently interfere in situ with ROS and free radical products are hard to nd. Consumption of large quantities of antioxidant vitamins, such as vitamins A, C or E is not effective or even harmful.…”

mentioning

confidence: 99%

Furan fatty acids efficiently rescue brain cells from cell death induced by oxidative stress

2013

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Treatment of rat brain C6 astroglioma cells with furan fatty acid F6 prior to exposure to hydrogen peroxide shows a strong protective effect of F6 against cell death resulting from oxidative stress. This protective effect is obtained only for F6 administered as a free fatty acid and with an intact furan ring. It is proposed that brain cells are rescued by F6 scavenging radicals elicited by lipid peroxidation within the cell membrane. Oxidative processes outside the cell membrane, such as protein carbonylation, are not affected by F6. Furan fatty acids such as those present in fish oils and marine organisms are likely beneficial for consumption in reducing the risk of diseases that have been implicated to arise from oxidative stress, such as Alzheimer's disease.

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Oxidative Stress Profiling:

Cited by 65 publications

References 115 publications

PKCγ knockout mouse lenses are more susceptible to oxidative stress damage

PKCγ knockout mouse lenses are more susceptible to oxidative stress damage

Burn and smoke inhalation injury in sheep depletes vitamin E: Kinetic studies using deuterated tocopherols

Furan fatty acids efficiently rescue brain cells from cell death induced by oxidative stress

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