Effect of malate on the development of rotenone-induced brain changes in Wistar and OXYS rats: An MRI study

Kolosova, N. G.; Akulov, Andrey E.; Stefanova, Natalia A.; Мошкин, М. П.; Савелов, А. А.; Koptyug, Igor V.; Panov, Alexander; Вавилин, В. А.

doi:10.1134/s0012496611020049

Cited by 17 publications

(15 citation statements)

References 10 publications

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“…Studies of animal models of human aging can allow researchers to precisely control these variables and may be used to assess the mechanisms and molecular pathways underlying any positive effects of antioxidant supplementation. Recently, we have shown that senescence-accelerated OXYS rats are suitable model for studies of aging and age-related cerebral dysfunctions (Loskutova and Kolosova, 2000;Loskutova and Zelenkina, 2002;Markova et al, 2003Markova et al, , 2005Sergeeva et al, 2006;Agafonova et al, 2010;Kolosova et al, 2011). We have found that the behavior of young OXYS rats is similar to the behavior of old Wistar rats.…”

Section: Introductionmentioning

confidence: 78%

Effects of Cistanche deserticola on behavior and signs of cataract and retinopathy in senescence-accelerated OXYS rats

Stefanova¹,

Фурсова²,

Sarsenbaev³

et al. 2011

Journal of Ethnopharmacology

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Section: Introductionmentioning

confidence: 78%

Effects of Cistanche deserticola on behavior and signs of cataract and retinopathy in senescence-accelerated OXYS rats

Stefanova¹,

Фурсова²,

Sarsenbaev³

et al. 2011

Journal of Ethnopharmacology

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“…These data also suggest that reverse electron transfer can be potential pharmacological target for the treatment of hypertension. It has been previously reported that malate attenuates reverse electron transfer and inhibits the production of mitochondrial ROS both in vitro and in vivo (30,42). We therefore performed additional studies in vivo infusing malate and mitoTEMPO after the onset of AngII-induced hypertension.…”

Section: Antihypertensive Effect Of Malate and Mitotempomentioning

confidence: 99%

Nox2-Induced Production of Mitochondrial Superoxide in Angiotensin II-Mediated Endothelial Oxidative Stress and Hypertension

Dikalov

Nazarewicz

Bikineyeva

et al. 2014

Antioxidants & Redox Signaling

270

203

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Aims: Angiotensin II (AngII)-induced superoxide (O 2 -) production by the NADPH oxidases and mitochondria has been implicated in the pathogenesis of endothelial dysfunction and hypertension. In this work, we investigated the specific molecular mechanisms responsible for the stimulation of mitochondrial O 2 -and its downstream targets using cultured human aortic endothelial cells and a mouse model of AngII-induced hypertension. Results: Western blot analysis showed that Nox2 and Nox4 were present in the cytoplasm but not in the mitochondria. Depletion of Nox2, but not Nox1, Nox4, or Nox5, using siRNA inhibits AngII-induced O 2 -production in both mitochondria and cytoplasm. Nox2 depletion in gp91phox knockout mice inhibited AngIIinduced cellular and mitochondrial O 2 -and attenuated hypertension. Inhibition of mitochondrial reverse electron transfer with malonate, malate, or rotenone attenuated AngII-induced cytoplasmic and mitochondrial O 2 -production. Inhibition of the mitochondrial ATP-sensitive potassium channel (mitoK

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“…Such lesions were not found in young Wistar rats. 41,63,67 Demyelination occurs both during healthy brain aging and in AD, but the magnitude of changes is significantly different. 68 With age, demyelination is detectable in Wistar rats, but in middle-aged and aged animals the number of demyelinating foci is smaller than that in age-matched OXYS rats (Fig.…”

Section: Signs Of Neurodegeneration In Oxys Ratsmentioning

confidence: 99%

Senescence-accelerated OXYS rats: A model of age-related cognitive decline with relevance to abnormalities in Alzheimer disease

et al. 2014

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Senescence-accelerated OXYS rats are an experimental model of accelerated aging that was established from wistar stock via selection for susceptibility to cataractogenic effects of a galactose-rich diet and via subsequent inbreeding of highly susceptible rats. Currently, we have the 102nd generation of OXYS rats with spontaneously developing cataract and accelerated senescence syndrome, which means early development of a phenotype similar to human geriatric disorders, including accelerated brain aging. in recent years, our group found strong evidence that OXYS rats are a promising model for studies of the mechanisms of brain aging and neurodegenerative processes similar to those seen in Alzheimer disease (AD). The manifestation of behavioral alterations and learning and memory deficits develop since the fourth week of age, i.e., simultaneously with first signs of neurodegeneration detectable on magnetic resonance imaging and under a light microscope. in addition, impaired long-term potentiation has been demonstrated in OXYS rats by the age of 3 months. with age, neurodegenerative changes in the brain of OXYS rats become amplified. we have shown that this deterioration happens against the background of overproduction of amyloid precursor protein (AβPP), accumulation of β-amyloid (Aβ), and hyperphosphorylation of the tau protein in the hippocampus and cortex. The development of AMDlike retinopathy in OXYS rats is also accompanied by increased accumulation of Aβ in the retina. These published data suggest that the OXYS strain may serve as a spontaneous rat model of AD-like pathology and could help to decipher the pathogenesis of AD.

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Effect of malate on the development of rotenone-induced brain changes in Wistar and OXYS rats: An MRI study

Cited by 17 publications

References 10 publications

Effects of Cistanche deserticola on behavior and signs of cataract and retinopathy in senescence-accelerated OXYS rats

Effects of Cistanche deserticola on behavior and signs of cataract and retinopathy in senescence-accelerated OXYS rats

Nox2-Induced Production of Mitochondrial Superoxide in Angiotensin II-Mediated Endothelial Oxidative Stress and Hypertension

Senescence-accelerated OXYS rats: A model of age-related cognitive decline with relevance to abnormalities in Alzheimer disease

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