4-Hydroxynonenal (4-HNE) is an α,β unsaturated hydroxyalkenal and an oxidative/nitrosative stress biomarker. 4-Hydroxynonenal is a substrate and an inhibitor of acetaldehyde dehydrogenase 2 (ALDH2). 4-Hydroxynonenal can modulate a number of signaling processes mainly through forming covalent adducts with nucleophilic functional groups in proteins, nucleic acids, and membrane lipids. 4-Hydroxynonenal plays an important role in cancer through mitochondria^[1][2][3].

4-Hydroxynonenal is both a substrate and an inhibitor of ALDH2; inhibition of ALDH2 by 4-Hydroxynonenal is reversible at low concentration and become irreversible when the concentration of 4-HNE reaches 10 µM^[1].
4-Hydroxynonenal can induce antioxidant defense mechanisms to restrain its own production and to enhance the cellular protection against oxidative stress^[1].
4-Hydroxynonenal, the product of lipid peroxidation, is mutagenic and genotoxic in viruses, bacteria and mammalian cells. It reacts with all four DNA bases but with different efficiency: G >C > A >T. 4-Hydroxynonenal-dG represents the best biomarker of the genotoxic effects of 4-Hydroxynonenal and these adducts are primarily found in nuclear DNA. A classic example of etiological relevance of 4-Hydroxynonenal-dG in human cancers is 4-Hydroxynonenal-dG induced p53 mutation. 4-Hydroxynonenal-dG adducts were preferentially formed at the third base of codon 249 in the p53 gene, causing gene mutation and affecting diverse biological processes including cell cycle arrest, apoptosis, DNA repair, and differentiation^[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Following 24 h after fluid percussion injury (FPI), the mouse brain tissue is analyzed for the expression level of NADPH oxidase 1 (NOX1), inducible nitric oxide synthase (iNOS), 4-Hydroxynonenal (4-HNE. Both wild-type (Nrf2^+/+) and Nrf2-deficient mice (Nrf2^−/−) results in increased expression of 4-Hydroxynonenal following 15 psi injury (moderate injury) when compared to uninjured Nrf2^+/+ and Nrf2^−/− mice. Similar to iNOS result, in Nrf2^−/− KO mice, the expression level of 4-Hydroxynonenal is significantly high when compared to corresponding injured and uninjured Nrf2^+/+ WT animals^[2].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

156.22

C₉H₁₆O₂

75899-68-2

Room temperature in continental US; may vary elsewhere.

Solution, -20°C, 2 years

DMSO : 100 mg/mL (640.12 mM; Need ultrasonic)

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

• 1.

  请依序添加每种溶剂： 10% DMSO    90% (20% SBE-β-CD in saline)

  Solubility: ≥ 2.5 mg/mL (16.00 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (16.00 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

  将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
• 2.

  请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

  Solubility: ≥ 2.08 mg/mL (13.31 mM); Clear solution

  此方案可获得 ≥ 2.08 mg/mL (13.31 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

  将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

• 3.

  请依序添加每种溶剂： 10% DMSO    90% corn oil

  Solubility: ≥ 2.08 mg/mL (13.31 mM); Clear solution

  此方案可获得 ≥ 2.08 mg/mL (13.31 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

  以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

• [1]. Zhong H, et al. Role of lipid peroxidation derived 4-hydroxynonenal (4-HNE) in cancer: focusing on mitochondria. Redox Biol. 2015;4:193-9.

  [2]. Csala M, et al. On the role of 4-hydroxynonenal in health and disease. Biochim Biophys Acta. 2015 May;1852(5):826-38.

  [3]. Bhowmick S, et al. Traumatic brain injury-induced downregulation of Nrf2 activates inflammatory response and apoptotic cell death. J Mol Med (Berl). 2019 Nov 22.