Whatsapp 93125-11015 For Details

Important Editorial Summary for UPSC Exam

24Jul
2024

Drug Used to Treat Clots Can Protect Against Cobra Venom Damage (GS Paper 3, Science)

Drug Used to Treat Clots Can Protect Against Cobra Venom Damage (GS Paper 3, Science)

Introduction

  • The red-spitting cobra (Naja pallida), a strikingly colored serpent native to Tanzania, poses a significant threat with its venomous capabilities.
  • Measuring around 1.2 meters in length, this snake uses its venom as a primary defense mechanism.
  • When threatened, it first tries to deter its attacker with a menacing display.
  • If this fails, it deploys its venom in a two-step attack: a venomous spray aimed at the eyes, nose, and mouth, followed by a bite that delivers a substantial quantity of venom into the victim’s bloodstream.

 

The Physiology of Cobra Venom

  • Venom Delivery Mechanism: The cobra’s venom glands are surrounded by muscles that, when contracted, forcefully eject venom onto the threat. This spray causes immediate pain and irritation, impairing the victim's ability to see or defend itself. The cobra then takes advantage of this distraction to bite, injecting a larger dose of venom.
  • Toxic Effects: Cobra venom contains a complex mixture of enzymes, proteins, and peptides that disrupt cellular functions and damage the nervous system. This can lead to paralysis, tissue necrosis, and in many cases, death. While the venom is lethal to most of its natural prey, humans can suffer severe injuries or permanent disabilities if bitten.

 

Challenges with Current Antivenoms

  • Prevalence and Impact: Venomous snakebites result in about 140,000 deaths annually, predominantly in tropical regions of Africa and Asia. Despite the high mortality rate, the treatment methods for snakebites remain outdated and inadequate.
  • Antivenom Production: The traditional method for producing antivenom involves immunizing domestic animals such as horses and sheep with small doses of snake venom. These animals develop antibodies against the venom, which are then extracted from their blood and used as antivenom. This process, established in the late 19th century, is fraught with challenges, including:
  • Production Difficulties: The process of producing and purifying antivenom is complex and labor-intensive.
  • Storage and Transportation: Antivenoms require careful storage and transportation under controlled conditions, which can be costly and logistically challenging.
  • Cost and Side Effects: Antivenoms are expensive and can cause severe allergic reactions or other adverse effects in patients.

 

Breakthrough Research on Tinzaparin

  • Study Overview: A groundbreaking study published in July 2024 in Science Translational Medicine explored the potential of tinzaparin, a drug commonly used as an anticoagulant (blood thinner), to counteract the effects of spitting cobra venom. The study was conducted by a team of researchers from Australia, the UK, Canada, and Costa Rica.
  • Findings: The researchers discovered that tinzaparin significantly reduces cellular damage caused by spitting cobra venom. In experiments, tinzaparin not only protected cells from venom-induced damage but also reduced skin damage in mice exposed to the venom.
  • Genetic Insights: The researchers linked the venom's toxicity to the presence of specific genes involved in the synthesis of heparan sulphate, a sugar compound essential for blood vessel formation and clotting. The absence of these genes in certain experimental models was associated with reduced venom toxicity.
  • Mechanism of Action: Tinzaparin mimics heparan sulphate and interferes with the venom's interaction with its cellular receptors. By introducing tinzaparin, the researchers effectively blocked the venom's ability to bind to and damage cells.

 

Blood Thinner as an Antidote

  • Hypothesis and Results: The study hypothesized that inhibiting the biological pathways involved in heparan sulphate synthesis could mitigate the venom’s toxic effects. Tinzaparin, by resembling heparan sulphate, was found to disrupt these pathways. This protective effect was observed when tinzaparin was administered immediately after venom exposure, and even up to an hour later.
  • Binding Mechanism: Tinzaparin works by binding to the venom molecules, preventing them from interacting with their receptors on the cells. This interaction disrupts the venom’s ability to cause damage.

 

Conclusion

  • The research into tinzaparin as a potential treatment for snakebite venom represents a significant advancement in addressing a long-neglected problem.
  • By applying modern techniques, including the CRISPR gene-editing approach, to study venom toxicity, scientists have opened new avenues for developing effective treatments.
  • This breakthrough could potentially revolutionize the field of antivenom research, offering a more accessible and less costly alternative to traditional antivenoms, and renewing global interest in understanding and combating snake venom toxicity.