Valproic acid promotes SOD2 acetylation: A potential mechanism of valproic acid-induced oxidative stress in developing systems

Due to the crucial role of oxidative stress on the pathophysiology of autism and the concept of synergistic effect, the benefit of the combined extract of purple rice and silkworm pupae (AP1) for autism disorder was the focus. Therefore, we aimed to determine the effect of AP1 on autistic-like behaviors, oxidative stress status, and histopathological change of cerebellum in valproic acid (VPA) rat model of autism. VPA was injected on postnatal day (PND) 14 and the animals were orally given AP1 at doses of 50, 100, and 200 mg·kg−1BW between PND 14 and PND 40. The autism-like behaviors were analyzed via hot-plate, rotarod, elevated plus-maze, learning, memory, and social behavior tests. Oxidative stress and the histological change in the cerebellum were assessed at the end of study. AP1 treated rats improved behaviors in all tests except that in hot-plate test. The improvement of oxidative stress and Purkinje cell loss was also observed in the cerebellum of VPA-treated rats. Our data suggest that AP1 partially reduced autism-like behaviors by improving oxidative stress and Purkinje cell loss. Further research is required to identify the active ingredients in AP1 and gender difference effect.

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Vinpocetine amended prenatal valproic acid induced features of ASD possibly by altering markers of neuronal function, inflammation, and oxidative stress

Autism Research ◽

10.1002/aur.2597 ◽

2021 ◽

Author(s):

Kanishk Luhach ◽

Giriraj T. Kulkarni ◽

Vijay P. Singh ◽

Bhupesh Sharma

Keyword(s):

Oxidative Stress ◽

Valproic Acid ◽

Neuronal Function ◽

And Oxidative Stress

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Valproic Acid II: Effects on Oxidative Stress, Mitochondrial Membrane Potential, and Cytotoxicity in Glutathione-Depleted Rat Hepatocytes

Toxicological Sciences ◽

10.1093/toxsci/kfi185 ◽

2005 ◽

Vol 86 (2) ◽

pp. 436-443 ◽

Cited By ~ 97

Author(s):

Vincent Tong ◽

Xiao Wei Teng ◽

Thomas K. H. Chang ◽

Frank S. Abbott

Keyword(s):

Oxidative Stress ◽

Valproic Acid ◽

Membrane Potential ◽

Mitochondrial Membrane Potential ◽

Mitochondrial Membrane ◽

Rat Hepatocytes

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Sulindac attenuates valproic acid-induced oxidative stress levels in primary cultured cortical neurons and ameliorates repetitive/stereotypic-like movement disorders in Wistar rats prenatally exposed to valproic acid

International Journal of Molecular Medicine ◽

10.3892/ijmm.2014.1996 ◽

2014 ◽

Vol 35 (1) ◽

pp. 263-270 ◽

Cited By ~ 9

Author(s):

YINGHUA ZHANG ◽

CAILING YANG ◽

GUOYAN YUAN ◽

ZHONGPING WANG ◽

WEIGANG CUI ◽

...

Keyword(s):

Oxidative Stress ◽

Valproic Acid ◽

Movement Disorders ◽

Cortical Neurons ◽

Wistar Rats ◽

Prenatally Exposed ◽

Stress Levels ◽

Cultured Cortical Neurons

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The role of oxidative stress in the cardiovascular actions of particulate air pollution

Biochemical Society Transactions ◽

10.1042/bst20140090 ◽

2014 ◽

Vol 42 (4) ◽

pp. 1006-1011 ◽

Cited By ~ 49

Author(s):

Mark R. Miller

Keyword(s):

Oxidative Stress ◽

Air Pollution ◽

Diesel Exhaust ◽

Vascular Function ◽

Cardiovascular Effects ◽

Increase Blood Pressure ◽

Potential Mechanism ◽

Particulate Air Pollution ◽

Cardiovascular Actions

Air pollution has been estimated to be responsible for several millions of deaths worldwide per year, the majority of which have been attributed to cardiovascular causes. The particulate matter in air pollution has been shown impair vascular function, increase blood pressure, promote thrombosis and impair fibrinolysis, accelerate the development of atherosclerosis, increase the extent of myocardial ischaemia, and increase susceptibility to myocardial infarction. The pathways underlying these effects are complex and poorly understood; however, particulate-induced oxidative stress repeatedly emerges as a potential mechanism in all of these detrimental cardiovascular actions. The present mini-review will use diesel exhaust as an example of a pollutant rich in combustion-derived nanoparticles, to describe the potential by which oxidative stress could drive the cardiovascular effects of air pollution.

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