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DL-Homocysteic acid

CAS# 504-33-6

DL-Homocysteic acid

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Chemical structure

DL-Homocysteic acid

3D structure

Chemical Properties of DL-Homocysteic acid

Cas No. 504-33-6 SDF Download SDF
PubChem ID 7018167 Appearance Powder
Formula C4H9NO5S M.Wt 183.18
Type of Compound Alkaloids Storage Desiccate at -20°C
Solubility Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
Chemical Name (2R)-2-azaniumyl-4-sulfonatobutanoate
SMILES C(CS(=O)(=O)[O-])C(C(=O)[O-])[NH3+]
Standard InChIKey VBOQYPQEPHKASR-GSVOUGTGSA-M
Standard InChI InChI=1S/C4H9NO5S/c5-3(4(6)7)1-2-11(8,9)10/h3H,1-2,5H2,(H,6,7)(H,8,9,10)/p-1/t3-/m1/s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of DL-Homocysteic acid

DescriptionDL-Homocysteic acid application disrupts calcium homeostasis and induces degeneration of spinal motor neurons in vivo.
TargetsCalcium Channel
In vitro

Effect of dl-homocysteic acid on W/O microemulsions of potassium naphthenate/1-octanol-n-heptane.[Pubmed: 15694443]

J Colloid Interface Sci. 2005 Mar 1;283(1):231-7.

The effect of DL-Homocysteic acid (DL-2-amino-4-sulfonobutyric acid) on W/O microemulsion of potassium naphthenate (80%) and naphthenic acid (20%) in mixed solvent (1-octanol and n-heptane) has been found in four phases: (1) Interaction between the amino acid molecules and the polar head groups of the surfactant through hydrogen bonding enhances solubilization in the aqueous cores. (2) The interaction results in the growth of the microemulsion droplets and the homogenization of the particle size distribution. (3) The microstructure of the solubilized water remains unchanged, except that the polarity of the interface is affected. (4) The transition point is reduced to lower water content. A possible mechanism is proposed.

In vivo

Cardiorespiratory effects of DL-homocysteic acid in caudal ventrolateral medulla.[Pubmed: 2646953]

Am J Physiol. 1989 Mar;256(3 Pt 2):H688-96.


METHODS AND RESULTS:
We carried out experiments in urethan-anesthetized rats to determine 1) whether increasing the activity of small groups of neurons in the caudal ventrolateral medulla (CVLM) by injecting picomoles of an excitatory amino acid altered cardiovascular and/or respiratory homeostasis and 2) whether the depressor responses after chemical excitation in the CVLM were elicited only from the immunohistochemically identified catecholamine-containing cell group. In discrete sites in the CVLM, unilateral injections of 1-12 nl (20-240 pmol) of DL-Homocysteic acid (DLH; 20 mM, pH 7.4) selectively or concomitantly inhibited arterial pressure, heart rate, and diaphragm electromyogram (EMG) activity. In the region in which chemical excitation slowed breathing, units were recorded extracellularly that discharged with respiratory periodicity. Sites where the smallest volumes of DLH decreased arterial pressure were located outside the immunohistochemically identified DBH-positive cell bodies.
CONCLUSIONS:
These data suggest that either the same or neighboring neurons in the CVLM are involved in the central neural circuitry for both cardiovascular and respiratory control and that cells other than the catecholaminergic cell group are important in medullary depressor responses.

DL-Homocysteic acid application disrupts calcium homeostasis and induces degeneration of spinal motor neurons in vivo.[Pubmed: 11935257]

Acta Neuropathol. 2002 May;103(5):428-36.

Excitotoxicity, autoimmunity and free radicals have been postulated to play a role in the pathomechanism of amyotrophic lateral sclerosis (ALS), the most frequent motor neuron disease. Altered calcium homeostasis has already been demonstrated in Cu/Zn superoxide dismutase transgenic animals, suggesting a role for free radicals in the pathogenesis of ALS, and in passive transfer experiments, modeling autoimmunity. These findings also suggested that yet-confined pathogenic insults, associated with ALS, could trigger the disruption of calcium homeostasis of motor neurons.
METHODS AND RESULTS:
To test the possibility that excitotoxic processes may also be able to increase calcium in motor neurons, we applied the glutamate analogue DL-Homocysteic acid to the spinal cord of rats in vivo and analyzed the calcium distribution of the motor neurons over a 24-h survival period by electron microscopy. Initially, an elevated cytoplasmic calcium level, with no morphological sign of degeneration, was noticed. Later, increasing calcium accumulation was seen in different cellular compartments with characteristic features of alteration at different survival times. This calcium accumulation in organelles was paralleled by their progressive degeneration, which culminated in cell death by the end of the observation time. These findings confirm that increased calcium also plays a role in excitotoxic lesion of motor neurons, in line with previous studies documenting the involvement of calcium ions in motor neuronal injury in other models of the disease as well as elevated calcium in biopsy samples from ALS patients.
CONCLUSIONS:
We suggest that intracellular calcium might be responsible for the interplay between the different pathogenic processes resulting in a uniform clinicopathological picture of the disease.

DL-Homocysteic acid Dilution Calculator

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Preparing Stock Solutions of DL-Homocysteic acid

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 5.4591 mL 27.2956 mL 54.5911 mL 109.1822 mL 136.4778 mL
5 mM 1.0918 mL 5.4591 mL 10.9182 mL 21.8364 mL 27.2956 mL
10 mM 0.5459 mL 2.7296 mL 5.4591 mL 10.9182 mL 13.6478 mL
50 mM 0.1092 mL 0.5459 mL 1.0918 mL 2.1836 mL 2.7296 mL
100 mM 0.0546 mL 0.273 mL 0.5459 mL 1.0918 mL 1.3648 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on DL-Homocysteic acid

Effect of dl-homocysteic acid on W/O microemulsions of potassium naphthenate/1-octanol-n-heptane.[Pubmed:15694443]

J Colloid Interface Sci. 2005 Mar 1;283(1):231-7.

The effect of DL-Homocysteic acid (DL-2-amino-4-sulfonobutyric acid) on W/O microemulsion of potassium naphthenate (80%) and naphthenic acid (20%) in mixed solvent (1-octanol and n-heptane) has been found in four phases: (1) Interaction between the amino acid molecules and the polar head groups of the surfactant through hydrogen bonding enhances solubilization in the aqueous cores. (2) The interaction results in the growth of the microemulsion droplets and the homogenization of the particle size distribution. (3) The microstructure of the solubilized water remains unchanged, except that the polarity of the interface is affected. (4) The transition point is reduced to lower water content. A possible mechanism is proposed.

DL-Homocysteic acid application disrupts calcium homeostasis and induces degeneration of spinal motor neurons in vivo.[Pubmed:11935257]

Acta Neuropathol. 2002 May;103(5):428-36.

Excitotoxicity, autoimmunity and free radicals have been postulated to play a role in the pathomechanism of amyotrophic lateral sclerosis (ALS), the most frequent motor neuron disease. Altered calcium homeostasis has already been demonstrated in Cu/Zn superoxide dismutase transgenic animals, suggesting a role for free radicals in the pathogenesis of ALS, and in passive transfer experiments, modeling autoimmunity. These findings also suggested that yet-confined pathogenic insults, associated with ALS, could trigger the disruption of calcium homeostasis of motor neurons. To test the possibility that excitotoxic processes may also be able to increase calcium in motor neurons, we applied the glutamate analogue DL-Homocysteic acid to the spinal cord of rats in vivo and analyzed the calcium distribution of the motor neurons over a 24-h survival period by electron microscopy. Initially, an elevated cytoplasmic calcium level, with no morphological sign of degeneration, was noticed. Later, increasing calcium accumulation was seen in different cellular compartments with characteristic features of alteration at different survival times. This calcium accumulation in organelles was paralleled by their progressive degeneration, which culminated in cell death by the end of the observation time. These findings confirm that increased calcium also plays a role in excitotoxic lesion of motor neurons, in line with previous studies documenting the involvement of calcium ions in motor neuronal injury in other models of the disease as well as elevated calcium in biopsy samples from ALS patients. We suggest that intracellular calcium might be responsible for the interplay between the different pathogenic processes resulting in a uniform clinicopathological picture of the disease.

Cardiorespiratory effects of DL-homocysteic acid in caudal ventrolateral medulla.[Pubmed:2646953]

Am J Physiol. 1989 Mar;256(3 Pt 2):H688-96.

We carried out experiments in urethan-anesthetized rats to determine 1) whether increasing the activity of small groups of neurons in the caudal ventrolateral medulla (CVLM) by injecting picomoles of an excitatory amino acid altered cardiovascular and/or respiratory homeostasis and 2) whether the depressor responses after chemical excitation in the CVLM were elicited only from the immunohistochemically identified catecholamine-containing cell group. In discrete sites in the CVLM, unilateral injections of 1-12 nl (20-240 pmol) of DL-Homocysteic acid (DLH; 20 mM, pH 7.4) selectively or concomitantly inhibited arterial pressure, heart rate, and diaphragm electromyogram (EMG) activity. In the region in which chemical excitation slowed breathing, units were recorded extracellularly that discharged with respiratory periodicity. Sites where the smallest volumes of DLH decreased arterial pressure were located outside the immunohistochemically identified DBH-positive cell bodies. These data suggest that either the same or neighboring neurons in the CVLM are involved in the central neural circuitry for both cardiovascular and respiratory control and that cells other than the catecholaminergic cell group are important in medullary depressor responses.

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