Effects of aminooxyacetic acid on hippocampal mitochondria in rats with chronic alcoholism: the analysis of learning and memory-related genes

Du, Aihua; Xuan, Dong; Dong, Jiaxing; Liu, Jia-Cong; Zhang, Yue; Fu, Pengyan; Qin, Haozhi; Li, Ruonan; Zhang, Ruiling

doi:10.31083/j.jin.2019.04.1119

Cited by 7 publications

(5 citation statements)

References 34 publications

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“…AOAA also induced complex changes in gene expression and antioxidant levels in the brain of the animals. [425,426] Male Swiss albino mice subjected to stroke (transient middle cerebral artery occlusion) in combination with remote ischemic preconditioning 50 mg/kg i.p. single dose AOAA suppressed the neuroprotective effect of remote ischemic preconditioning.…”

Section: Animal Model Dose Of Aoaa Effects Of Aoaa; Proposed Mechanis...mentioning

confidence: 99%

“…For example, if we return to the discussion concerning cysteine aminotransferase/aspartate aminotransferase (see above) it should be emphasized that when, aspartate is used as a substrate, this enzyme catalyzes the production of oxaloacetate, thus bridging the Krebs cycle with the urea cycle and gluconeogenesis through the malate/aspartate shuttle (MAS). In fact, in a separate field of biochemistry (that almost never communicates with the "H 2 S Universe"), AOAA has been often employed to pharmacologically inhibit GOT to modulate the above metabolic pathways; in this context, AOAA has been found to suppress cellular metabolism in various experimental contexts ranging from cardiovascular disease to cancer [88,296,320,369,389,394,423,426,[469][470][471] (see also: Table 3). Figure 12 depicts some key AOAA-inhibitable metabolic pathways (in the "H 2 S Universe" and beyond) and their potential synergistic interactions in support of tumor cell bioenergetics.…”

Section: The Lack Of Aoaa's Selectivity As a Pharmacological Inhibitormentioning

confidence: 99%

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Cystathionine-β-synthase: Molecular Regulation and Pharmacological Inhibition

et al. 2020

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Cystathionine-β-synthase (CBS), the first (and rate-limiting) enzyme in the transsulfuration pathway, is an important mammalian enzyme in health and disease. Its biochemical functions under physiological conditions include the metabolism of homocysteine (a cytotoxic molecule and cardiovascular risk factor) and the generation of hydrogen sulfide (H2S), a gaseous biological mediator with multiple regulatory roles in the vascular, nervous, and immune system. CBS is up-regulated in several diseases, including Down syndrome and many forms of cancer; in these conditions, the preclinical data indicate that inhibition or inactivation of CBS exerts beneficial effects. This article overviews the current information on the expression, tissue distribution, physiological roles, and biochemistry of CBS, followed by a comprehensive overview of direct and indirect approaches to inhibit the enzyme. Among the small-molecule CBS inhibitors, the review highlights the specificity and selectivity problems related to many of the commonly used “CBS inhibitors” (e.g., aminooxyacetic acid) and provides a comprehensive review of their pharmacological actions under physiological conditions and in various disease models.

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Section: Animal Model Dose Of Aoaa Effects Of Aoaa; Proposed Mechanis...mentioning

confidence: 99%

Section: The Lack Of Aoaa's Selectivity As a Pharmacological Inhibitormentioning

confidence: 99%

Cystathionine-β-synthase: Molecular Regulation and Pharmacological Inhibition

et al. 2020

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“…The enzyme catalase is found mainly within peroxisomes, and to a lesser extent, in mitochondria. Until now, it was described in heart [ 100 ] liver [ 101 ], and cerebral hippocampus [ 102 ]. Catalase breaks down two hydrogen peroxide molecules into one molecule of oxygen [ 103 ] and two molecules of water in a two-step reaction [ 104 ].…”

Section: Mitochondrial Antioxidant Systemmentioning

confidence: 99%

Mitochondrial Management of Reactive Oxygen Species

Napolitano

Fasciolo²,

Venditti³

2021

Antioxidants

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Mitochondria in aerobic eukaryotic cells are both the site of energy production and the formation of harmful species, such as radicals and other reactive oxygen species, known as ROS. They contain an efficient antioxidant system, including low-molecular-mass molecules and enzymes that specialize in removing various types of ROS or repairing the oxidative damage of biological molecules. Under normal conditions, ROS production is low, and mitochondria, which are their primary target, are slightly damaged in a similar way to other cellular compartments, since the ROS released by the mitochondria into the cytosol are negligible. As the mitochondrial generation of ROS increases, they can deactivate components of the respiratory chain and enzymes of the Krebs cycle, and mitochondria release a high amount of ROS that damage cellular structures. More recently, the feature of the mitochondrial antioxidant system, which does not specifically deal with intramitochondrial ROS, was discovered. Indeed, the mitochondrial antioxidant system detoxifies exogenous ROS species at the expense of reducing the equivalents generated in mitochondria. Thus, mitochondria are also a sink of ROS. These observations highlight the importance of the mitochondrial antioxidant system, which should be considered in our understanding of ROS-regulated processes. These processes include cell signaling and the progression of metabolic and neurodegenerative disease.

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“…Alcohol exposure consistently produced deficits in Y-maze performance. A 28-day forced alcohol exposure via spiked drinking water impaired spatial and learning memory in rats ( Du et al, 2019 ). In mice, a longer exposure of 42 days (5 mg/kg daily i.p.)…”

Section: Methods Of Administrationmentioning

confidence: 99%

The Effect of Chronic Alcohol on Cognitive Decline: Do Variations in Methodology Impact Study Outcome? An Overview of Research From the Past 5 Years

Charlton

Perry

2022

Front. Neurosci.

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Excessive alcohol use is often associated with accelerated cognitive decline, and extensive research using animal models of human alcohol consumption has been conducted into potential mechanisms for this relationship. Within this literature there is considerable variability in the types of models used. For example, alcohol administration style (voluntary/forced), length and schedule of exposure and abstinence period are often substantially different between studies. In this review, we evaluate recent research into alcohol-induced cognitive decline according to methodology of alcohol access, as well as cognitive behavioral task employed. Our aim was to query whether the nature and severity of deficits observed may be impacted by the schedule and type of alcohol administration. We furthermore examined whether there is any apparent relationship between the amount of alcohol consumed and the severity of the deficit, as well as the potential impact of abstinence length, and other factors such as age of administration, and sex of subject. Over the past five years, researchers have overwhelmingly used non-voluntary methods of intake, however deficits are still found where intake is voluntary. Magnitude of intake and type of task seem most closely related to the likelihood of producing a deficit, however even this did not follow a consistent pattern. We highlight the importance of using systematic and clear reporting styles to facilitate consistency across the literature in this regard. We hope that this analysis will provide important insights into how experimental protocols might influence findings, and how different patterns of consumption are more or less likely to produce an addiction-vulnerable cognitive phenotype in animal models.

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Effects of aminooxyacetic acid on hippocampal mitochondria in rats with chronic alcoholism: the analysis of learning and memory-related genes

Cited by 7 publications

References 34 publications

Cystathionine-β-synthase: Molecular Regulation and Pharmacological Inhibition

Cystathionine-β-synthase: Molecular Regulation and Pharmacological Inhibition

Mitochondrial Management of Reactive Oxygen Species

The Effect of Chronic Alcohol on Cognitive Decline: Do Variations in Methodology Impact Study Outcome? An Overview of Research From the Past 5 Years

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