Production of reactive oxygen by mitochondria from normoxic and hypoxic rat heart tissue

Paraidathathu, Thomas; Groot, Herbert de; Kehrer, James P.

doi:10.1016/0891-5849(92)90176-h

Cited by 98 publications

(30 citation statements)

References 37 publications

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“…These sensitized cells exhibited significantly increased levels of apoptosis compared with control cells that were not challenged with IP 3 stimuli (Szalai et al, 1999). Mitochondrial Ca 2ϩ uptake has also been shown to stimulate reactive oxygen species (ROS) production (Chacon and Acosta, 1991;Paraidathathu et al, 1992;Richter, 1993), and mitochondrial Ca 2ϩ cycling can result in a self-propagating cascade that leads to loss of ATP and ⌬⌿ (Richter, 1997). Furthermore, oxidative stress induced by t-BuOOH has itself been reported to increase mitochondrial free Ca 2ϩ , ROS formation, and stimulate opening of the MPT (Byrne et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

“…In fact, our data quite clearly demonstrate that ⌬⌿ is increased by mitochondrial Ca 2ϩ uptake. It is generally presumed that metabolic activity generates oxidative stress via an increase in the production of ROS (Paraidathathu et al, 1992;Dawson et al, 1993;Richter, 1997). This only occurs when there is an imbalance between the generation and scavenging of ROS.…”

Section: Discussionmentioning

confidence: 99%

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Purinergic Receptor-Stimulated IP3-Mediated Ca2+ Release Enhances Neuroprotection by Increasing Astrocyte Mitochondrial Metabolism during Aging

Wu¹,

Holstein²,

Upadhyay³

et al. 2007

Journal of Neuroscience

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Astrocytes play an essential role in the maintenance and protection of the brain, which we reported was diminished with age. Here, we demonstrate that activation of a purinergic receptor (P2Y-R) signaling pathway, in astrocytes, significantly increases the resistance of astrocytes and neurons to oxidative stress. Interestingly, P2Y-R activation in old astrocytes increased their resistance to oxidative stress to levels that were comparable with stimulated young astrocytes. P2Y-R enhanced neuroprotection was blocked by oligomycin and by Xestospongin C, inhibitors of the ATP synthase and of inositol (1,4,5) triphosphate (IP 3 ) binding to the IP 3 receptor, respectively. Treatment of astrocytes with a membrane permeant analog of IP 3 also protected astrocytes against oxidative stress. These data indicate that P2Y-R enhanced astrocyte neuroprotection is mediated by a Ca 2ϩ -dependent increase in mitochondrial metabolism. These data also reveal a signaling pathway that can rapidly respond to central energy needs throughout the aging process.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Purinergic Receptor-Stimulated IP3-Mediated Ca2+ Release Enhances Neuroprotection by Increasing Astrocyte Mitochondrial Metabolism during Aging

Wu¹,

Holstein²,

Upadhyay³

et al. 2007

Journal of Neuroscience

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“…This alternate source appears to be much more basic-the resumption of mitochondrial respiration itself (Ambrosio et al, 1993). As intracellular calcium levels rise in energy-compromised ischemia tissues, the calcium is avidly taken up by the mitochondria leading to uncoupling, futile cycling, and increase production of superoxide (Paraidathathu et al, 1992). This mechanism of reoxygenation-induced superoxide production is likely common to all mammalian cells.…”

Section: Ischemia/reperfusion Injurymentioning

confidence: 99%

Superoxide Dismutase, Lipid Peroxidation, and Bell-Shaped Dose Response Curves

McCord

2008

Dose-Response

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h Cellular metabolism generates the cytotoxic superoxide free radical, O 2 · -, and a family of enzymes called superoxide dismutases (SOD) protects us from O 2 · -by catalyzing its conversion to O 2 and H 2 O 2 . Superoxide production increases in a wide variety of pathological states, especially those involving inflammation or ischemic injury. Most of the literature has described systems wherein added or over expressed SOD produced beneficial effects, yet in some circumstances SOD provided no benefit, or was clearly detrimental, exacerbating cell injury or death. When broad dose-response studies were finally possible in models of reperfusion injury in the isolated heart, hormesis became clear. We propose that the mechanisms underlying the hormesis are related to the paradoxical abilities of the superoxide radical to serve as both an initiator and a terminator of the free radicalmediated chain reaction that results in lipid peroxidation. Lipid peroxidation is a universal feature of oxidative stress, causing loss of cellular structure and function. Under any given conditions, the optimal concentration of SOD is that which decreases chain initiation without elimination of the chain termination properties of the radical, resulting in a minimum of net lipid peroxidation. Mathematical modeling of this hypothesis yields predictions fully consistent with observed laboratory data.

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“…Next, we examined if our developed method enables measurement of oxidative damage from ROS produced in the mitochondria, which are considered to be the main site for ROS production (Paraidathathu et al, 1992). N2, sod-1 and sod-2 mutant strains were exposed to rotenone, a Complex I inhibitor of the mitochondrial electron transport chain which enhances mitochondrial ROS production .…”

Section: Elegansmentioning

confidence: 99%

Quantification of in vivo oxidative damage in Caenorhabditis elegans during aging by endogenous F3‐isoprostane measurement

et al. 2013

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SummaryOxidative damage is thought to be a major cause in development of pathologies and aging. However, quantification of oxidative damage is methodologically difficult. Here, we present a robust liquid chromatography-tandem mass spectrometry (LC-MS/MS) approach for accurate, sensitive, and linear in vivo quantification of endogenous oxidative damage in the nematode Caenorhabditis elegans, based on F3-isoprostanes. F3-isoprostanes are prostaglandin-like markers of oxidative damage derived from lipid peroxidation by Reactive Oxygen Species (ROS). Oxidative damage was quantified in whole animals and in multiple cellular compartments, including mitochondria and peroxisomes. Mutants of the mitochondrial electron transport proteins mev-1 and clk-1 showed increased oxidative damage levels. Furthermore, analysis of Superoxide Dismutase (sod) and Catalase (ctl) mutants uncovered that oxidative damage levels cannot be inferred from the phenotype of resistance to pro-oxidants alone and revealed high oxidative damage in a small group of chemosensory neurons. Longitudinal analysis of aging nematodes revealed that oxidative damage increased specifically with postreproductive age. Remarkably, aging of the stress-resistant and long-lived daf-2 insulin/IGF-1 receptor mutant involved distinct daf-16-dependent phases of oxidative damage including a temporal increase at young adulthood. These observations are consistent with a hormetic response to ROS.

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Production of reactive oxygen by mitochondria from normoxic and hypoxic rat heart tissue

Cited by 98 publications

References 37 publications

Purinergic Receptor-Stimulated IP3-Mediated Ca2+ Release Enhances Neuroprotection by Increasing Astrocyte Mitochondrial Metabolism during Aging

Purinergic Receptor-Stimulated IP3-Mediated Ca2+ Release Enhances Neuroprotection by Increasing Astrocyte Mitochondrial Metabolism during Aging

Superoxide Dismutase, Lipid Peroxidation, and Bell-Shaped Dose Response Curves

Quantification of in vivo oxidative damage in Caenorhabditis elegans during aging by endogenous F3‐isoprostane measurement

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