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應用
NAD-ADH Reagent Multiple Test Vial has been used to determine the alcohol content in blood. It has also been used to detect ethanol levels in mice.
生化／生理作用
Alcohol dehydrogenase (ADH) catalyzes the oxidation of alcohol to acetaldehyde with the simultaneous reduction of nicotinamide adenine dinucleotide (NAD) to NADH. The consequent increase in absorbance at 340 nm is directly proportional to alcohol concentration in the sample.
其他說明
Vial contains ≥10 μmol of nicotinamide adenine dinucleotide (NAD) and ≥800 units of yeast alchohol dehydrogenase (ADH), buffer salts, and stabilizers.
訊號詞
Danger
危險聲明
危險分類
Resp. Sens. 1
儲存類別代碼
11 - Combustible Solids
水污染物質分類（WGK）
WGK 3
閃點（°F）
Not applicable
閃點（°C）
Not applicable
個人防護裝備
Eyeshields, Gloves, type N95 (US)
其他客户在看
Ana M Romero et al.
Neurotoxicity research, 29(1), 69-79 (2015-08-13)
Chronic alcohol consumption may cause neurodevelopmental and neurodegenerative disorders. Alcohol neurotoxicity is associated with the production of acetaldehyde and reactive oxygen species that induce oxidative DNA damage. However, the molecular mechanisms by which ethanol disturbs the DNA damage response (DDR)
Denys V Volgin
Neuroscience letters, 439(2), 182-186 (2008-06-03)
Prenatal alcohol exposure (AE) is associated with lasting abnormalities of sleep and motor development, but the underlying mechanisms are unknown. We hypothesized that AE alters development of GABAergic signaling in the hypothalamic regions important for the control of sleep and
A rapid enzymatic method for estimating ethanol in body fluids.
D Jones et al.
Clinical chemistry, 16(5), 402-407 (1970-05-01)
Isabelle Larosche et al.
The Journal of pharmacology and experimental therapeutics, 332(3), 886-897 (2009-12-18)
Alcohol consumption increases reactive oxygen species (ROS) formation, which can damage mitochondrial DNA (mtDNA) and alter mitochondrial function. To test whether manganese superoxide dismutase (MnSOD) modulates acute alcohol-induced mitochondrial alterations, transgenic MnSOD-overexpressing (MnSOD(+++)) mice, heterozygous knockout (MnSOD(+/-)) mice, and wild-type
Tatsuro Kumada et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 26(3), 742-756 (2006-01-20)
The brains of fetal alcohol syndrome patients exhibit impaired neuronal migration, but little is known about the mechanisms underlying this abnormality. Here we show that Ca2+ signaling and cyclic nucleotide signaling are the central targets of alcohol action in neuronal
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