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Oxidopamine (hydrobromide)


CAS No. : 636-00-0

(Synonyms: 6-Hydroxydopamine hydrobromide; 6-OHDA hydrobromide)

636-00-0
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Cat. No. : HY-B1081A
M.Wt: 250.09
Formula: C8H12BrNO3
Purity: >98 %
Solubility: H2O : 20 mg/mL (ultrasonic);DMSO : 50 mg/mL (ultrasonic)
Introduction of 636-00-0 :

Oxidopamine (6-OHDA) hydrobromide is an antagonist of the neurotransmitter dopamine. Oxidopamine hydrobromide is a widely used neurotoxin and selectively destroys dopaminergic neurons. Oxidopamine hydrobromide promotes COX-2 activation, leading to PGE2 synthesis and pro-inflammatory cytokine IL-1β secretion. Oxidopamine hydrobromide can be used for the research of Parkinson’s disease (PD), attention-deficit hyperactivity disorder (ADHD), and Lesch-Nyhan syndrome[1][2][3][4]. In Vitro: Oxidopamine hydrobromide (0-500 μM, 24 h) decreases the viability of both Neuro-2a cells and SH-SY5Y cells in a concentration-dependent manner[1].
Oxidopamine hydrobromide (75-150 μM, 0-24 h) induces COX-2 expression and nuclear translocation[1].
Oxidopamine hydrobromide (75-150 μM, 0-24 h) causes PGE2 biosynthesis and pro-inflammatory cytokine IL-1β production[1].
Oxidopamine hydrobromide (0-150 μM, 12 h) induces apoptosis and mitochondrial membrane depolarization of pheochromocytoma PC12 cells[3].
Oxidopamine hydrobromide (75 μM, 0-12 h) induces p38 phosphorylation[3]. In Vivo: Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.

Oxidopamine (6-OHDA) hydrobromide can induce Parkinson's disease models[5][6].

Induction of Parkinson's disease model[5][6][7]
Background
The chemical structure of Oxidopamine (6-OHDA) hydrobromide is similar to dopamine (DA), enabling it to compete with DA for uptake sites and be subsequently taken into cells. Once inside the cells, oxidopamine hydrochloride can be oxidized and decomposed, generating reactive oxygen species, which further produce oxygen free radicals through MAO (monoamine oxidase) or directly cause mitochondrial dysfunction, leading to the death of dopaminergic neurons.
Specific Modeling Methods
Rat: Sprague-Dawley (SD) • Male • 200-250 g;
Administration: 5μg/2μL/site • stereotaxically injected in the fight striatum • single dose.
Solvent: dissolved in 0.1%-0.2% Ascorbic acid in PBS or 0.1%-0.2% Ascorbic acid in saline.
Note
Oxidopamine hydrobromide is commonly dissolved in 0.1% Ascorbic acid in saline or 0.1% Ascorbic acid in PBS in the literature. L‑Ascorbic acid (HY‑B0166) (ascorbic acid) has been reported to possess antioxidant properties, which can prevent the degradation of Oxidopamine.
(1) Lesions were made by the unilateral injection of Oxidopamine hydrobromide (5 μg in 2 μl/site) into the right striatum at the two coordinates:
① AP, 0.7; L, 3.0; DV, 5.5 and 4.5 mm from Bregma.
② AP, 0.2; L, 2.6; DV, 5.5 and 4.5 mm from Bregma.
The two coordinates were injected Oxidopamine hydrobromide 10 μg in 4 μl/2 sites.
(2) Oxidopamine hydrobromide was prepared freshly in dark to avoid autooxidation, and was administered using a 5 μl microinjector at a rate of 0.5 μl/min. The syringe was left in place for 5 min before slowly retracting it to allow for toxin diffusion and prevent the toxin reflux.
(3) On the 56th day after the injury, the animals were decapitated under deep halothane anesthesia. Their brains were quickly removed from the skull, rinsed with chilled saline, and tissue samples containing the caudate-putamen head were dissected from both the lesioned and unlesioned striata on ice.
(4) The animals were housed in an environment with a 12-hour light/dark cycle, with the temperature maintained at 22-23°C. They were allowed free access to food and tap water.
Modeling Indicators
Behavioral monitoring: Rats exhibit rotation with a rotation count greater than 210 r/30 min. Molecular changes: Elevated levels of COX-2, TNF-α mRNA, and COX-2 protein. Histopathological changes: Chromatin condensation into clumps around the nucleus, along with evident mitochondrial swelling and vacuolation. Induced nigrostriatal nerve terminal lesions. Decreased striatal dopamine levels and reduced number of tyrosine hydroxylase immunoreactive cells in the ipsilateral substantia nigra, accompanied by long-term significant atrophy of remaining dopaminergic neurons.
Opposite Product(s): Resveratrol (HY-16561)

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