Drug used to treat clots can protect against cobra venom damage
- July 24, 2024
- Posted by: OptimizeIAS Team
- Category: DPN Topics
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Drug used to treat clots can protect against cobra venom damage
Subject: Sci
Sec: Health
Context:
- Researchers have found that Tinzaparin has significantly reduced damage to human cells due to spitting cobra venom.
What is snake venom and how does it kill cells?
- Snake venom is a complex mixture of proteins, enzymes, peptides, and other bioactive molecules produced by venomous snakes.
- Peptides found in venom include cytotoxins, cardiotoxins, and neurotoxins, which target specific physiological systems in prey.
- Once the toxins are injected, they can work in several ways depending on the type of snake and toxins like hemotoxins, neurotoxins,myotoxins.
How can blood thinners be an antidote?
- Using CRISPR-Cas9 technique researchers conferred that the genes were involved in facilitating the venom’s effects on normal human cells and the resistance to spitting cobra venom had been conferred by the absence of a gene.
- Investigation revealed that many of these genes were involved in the synthesis of a sugar compound called heparan sulfate, which is known to regulate the formation of blood vessels and clots in the human body.
- The researchers hypothesize that if the venom’s toxicity depended on the biological pathway that synthesized heparan sulfate, artificially stopping this pathway could ameliorate the venom’s toxic effects.
- One way of doing so is to introduce molecules that closely resemble heparan sulfate ex tinzaparin, a drug used to treat serious blood clots.
- As the body senses an excess of these molecules, it shuts down the pathways responsible for heparan sulfate synthesis.
- Researchers introduced tinzaparin immediately after subjecting cells to the snake venom, the cells survived.
- Tinzaparin could protect these cells even when it was introduced an hour after the cells had been exposed to the venom.
- Further experiments revealed that tinzaparin worked by blocking the interaction between the venom and its receptor in the cell by binding to venom molecules.