Veratridine: Difference between revisions

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'''Veratridine''' is a steroid-derived alkaloid from plants in the Liliaceae family that functions as a neurotoxin by preventing the inactivation of [[sodium channels]]. It is used in biochemical experiments for its effects on sodium channels, which have been well-characterized.
{{Short description|A steroid-derived alkaloid toxin}}
{{Chembox
| ImageFile = Veratridine_structure.png
| ImageSize = 250px
| ImageAlt = Structural formula of Veratridine
| IUPACName = (3_, 4_, 5_, 22_)-Veratraman-3,4,5,22-tetrol
}}


==Chemical Structure==
'''Veratridine''' is a steroid-derived [[alkaloid]] toxin that affects [[sodium channel]]s in [[nerve cell]]s. It is primarily found in the seeds of the [[Schoenocaulon]] plant, commonly known as sabadilla, and in the [[Liliaceae]] family of plants. Veratridine is known for its ability to increase the permeability of sodium channels, leading to prolonged depolarization of the nerve cell membrane.
Veratridine is a complex steroid-derived alkaloid. It is composed of a steroid nucleus with three additional rings attached. The molecule also contains several hydroxyl groups and a lactone ring.


==Sources==
==Chemical structure==
Veratridine is found in plants in the Liliaceae family, including species of the genera ''Veratrum'' and ''Schoenocaulon''. These plants are native to North America and parts of Europe and Asia.
Veratridine is a complex molecule with a steroidal backbone. The structure of veratridine includes multiple hydroxyl groups and a distinctive arrangement of carbon rings. The molecular formula is C36H51NO11. The structure is depicted in the image [[File:Veratridine_structure.png|thumb|right|250px|Structural formula of Veratridine]].


==Mechanism of Action==
==Mechanism of action==
Veratridine acts as a neurotoxin by binding to [[voltage-gated sodium channels]] on neurons. This binding prevents the inactivation of the sodium channels, leading to a prolonged influx of sodium ions into the neuron. This results in a prolonged depolarization of the neuron, which can lead to cell death.
Veratridine acts by binding to the [[voltage-gated sodium channel]]s on the neuronal cell membrane. This binding causes the channels to remain open longer than usual, which results in a continuous influx of sodium ions into the cell. The prolonged depolarization prevents the cell from returning to its resting state, leading to increased neuronal excitability. The specific binding site of veratridine on the sodium channel is illustrated in the image [[File:Veratridine_binding_site.png|thumb|right|250px|Veratridine binding site on sodium channels]].


==Uses==
==Toxicity and effects==
In biochemical research, veratridine is used for its effects on sodium channels. It is often used in experiments to study the properties of these channels, as its effects on them have been well-characterized.
The toxic effects of veratridine are primarily due to its action on the nervous system. Symptoms of veratridine poisoning include [[nausea]], [[vomiting]], [[diarrhea]], [[muscle weakness]], and [[convulsions]]. In severe cases, it can lead to [[respiratory failure]] and [[death]]. The compound is used in research to study the function of sodium channels and the effects of their prolonged activation.


==Toxicity==
==Applications in research==
Veratridine is highly toxic and can cause a variety of symptoms if ingested or absorbed through the skin. These can include nausea, vomiting, abdominal pain, and in severe cases, seizures or death.
Veratridine is utilized in [[neuroscience]] research to investigate the properties of sodium channels and their role in [[neurotransmission]]. It serves as a tool to understand the mechanisms of [[nerve impulse]] propagation and the effects of channelopathies, which are disorders caused by dysfunctional ion channels.


==Treatment==
==Related compounds==
Treatment for veratridine poisoning is primarily supportive, with the goal of managing symptoms and preventing complications. This can include measures such as fluid replacement, seizure control, and in some cases, the use of drugs to counteract the effects of the toxin.
Veratridine is structurally related to other steroidal alkaloids, such as [[veratrine]] and [[cevadine]]. These compounds share similar mechanisms of action and are also found in plants of the Liliaceae family. The comparison of steroid and veratridine ring backbones is shown in the image [[File:Steroid_and_Veratridine_Ring_Backbones.png|thumb|right|250px|Comparison of steroid and veratridine ring backbones]].


==See Also==
==Related pages==
* [[Sodium channels]]
* [[Sodium channel]]
* [[Alkaloid]]
* [[Neurotoxin]]
* [[Neurotoxin]]
* [[Veratrum]]
* [[Schoenocaulon]]


[[Category:Toxins]]
[[Category:Alkaloids]]
[[Category:Alkaloids]]
[[Category:Neurotoxins]]
[[Category:Neurotoxins]]
[[Category:Biochemistry]]
[[Category:Sodium channel modulators]]
 
<gallery>
{{stub}}
File:Veratridine_structure.png|Veratridine structure
File:Steroid_and_Veratridine_Ring_Backbones.png|Steroid and Veratridine ring backbones
File:Veratridine_binding_site.png|Veratridine binding site
</gallery>

Latest revision as of 03:55, 18 February 2025

A steroid-derived alkaloid toxin


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Veratridine is a steroid-derived alkaloid toxin that affects sodium channels in nerve cells. It is primarily found in the seeds of the Schoenocaulon plant, commonly known as sabadilla, and in the Liliaceae family of plants. Veratridine is known for its ability to increase the permeability of sodium channels, leading to prolonged depolarization of the nerve cell membrane.

Chemical structure[edit]

Veratridine is a complex molecule with a steroidal backbone. The structure of veratridine includes multiple hydroxyl groups and a distinctive arrangement of carbon rings. The molecular formula is C36H51NO11. The structure is depicted in the image

Structural formula of Veratridine

.

Mechanism of action[edit]

Veratridine acts by binding to the voltage-gated sodium channels on the neuronal cell membrane. This binding causes the channels to remain open longer than usual, which results in a continuous influx of sodium ions into the cell. The prolonged depolarization prevents the cell from returning to its resting state, leading to increased neuronal excitability. The specific binding site of veratridine on the sodium channel is illustrated in the image

Veratridine binding site on sodium channels

.

Toxicity and effects[edit]

The toxic effects of veratridine are primarily due to its action on the nervous system. Symptoms of veratridine poisoning include nausea, vomiting, diarrhea, muscle weakness, and convulsions. In severe cases, it can lead to respiratory failure and death. The compound is used in research to study the function of sodium channels and the effects of their prolonged activation.

Applications in research[edit]

Veratridine is utilized in neuroscience research to investigate the properties of sodium channels and their role in neurotransmission. It serves as a tool to understand the mechanisms of nerve impulse propagation and the effects of channelopathies, which are disorders caused by dysfunctional ion channels.

Related compounds[edit]

Veratridine is structurally related to other steroidal alkaloids, such as veratrine and cevadine. These compounds share similar mechanisms of action and are also found in plants of the Liliaceae family. The comparison of steroid and veratridine ring backbones is shown in the image

Comparison of steroid and veratridine ring backbones

.

Related pages[edit]