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What Neurotoxin Is Present in Lathyrus?

3 min read

Epidemics of neurolathyrism, a paralytic disease, have been documented throughout history following prolonged consumption of certain Lathyrus species. The primary neurotoxin responsible for this condition is β-N-oxalyl-L-α,β-diaminopropionic acid, commonly known as ODAP.

Quick Summary

The legume genus Lathyrus contains the neurotoxin β-ODAP, which causes neurolathyrism, a paralyzing neurological disease, upon chronic overconsumption. The toxin acts as an excitotoxin, leading to motor neuron death, particularly affecting the lower limbs.

Key Points

  • ODAP is the Neurotoxin: The neurotoxin present in Lathyrus species is β-N-oxalyl-L-α,β-diaminopropionic acid (β-ODAP).

  • Cause of Neurolathyrism: Chronic consumption of large quantities of Lathyrus seeds containing β-ODAP leads to neurolathyrism, a motor neuron disease.

  • Excitotoxic Mechanism: β-ODAP acts as an excitotoxin, overstimulating glutamate receptors and causing motor neuron death, particularly in the spinal cord.

  • Neurological Symptoms: Symptoms include muscle weakness, cramps, spastic paraparesis, and in severe cases, irreversible paralysis of the legs.

  • Affected Populations: The disease is most prevalent in areas with famine or drought, where grass pea is consumed as a staple due to its resilience.

  • Traditional Detoxification: Methods like soaking and boiling can reduce the β-ODAP content, but they are not fully effective and depend on resource availability.

  • Modern Solutions: Plant breeding efforts have successfully developed low-toxin varieties of grass pea to reduce the risk of neurolathyrism.

In This Article

The Neurotoxin β-ODAP: The Culprit in Lathyrus

The neurotoxin present in several species of the legume genus Lathyrus, most notably Lathyrus sativus or grass pea, is β-N-oxalyl-L-α,β-diaminopropionic acid (β-ODAP). Also referred to as BOAA, this non-protein amino acid is the direct cause of a debilitating neurodegenerative condition in humans and animals called neurolathyrism. This condition arises when large quantities of Lathyrus seeds are consumed over a prolonged period, especially in regions experiencing famine or drought where the hardy crop is a main food source. β-ODAP acts as an excitotoxin, overstimulating glutamate receptors in the central nervous system, which leads to neuronal damage and death.

The Mechanism of Neurotoxicity

Unlike acute poisoning, neurolathyrism is a chronic condition that develops over time with consistent exposure to high levels of β-ODAP. The toxin's primary mechanism of action is linked to its structural resemblance to the neurotransmitter glutamate. By binding to and over-activating specific glutamate receptors, particularly the AMPA-activated receptors, β-ODAP causes an influx of calcium into motor neurons. This excess calcium triggers a cascade of events that culminates in mitochondrial damage, oxidative stress, and programmed cell death (apoptosis).

Key aspects of β-ODAP's toxic action include:

  • Excitotoxicity: Overstimulation of nerve cells leading to their eventual death.
  • Targeted damage: The toxin preferentially affects motor neurons in the spinal cord and areas of the brain controlling the legs, leading to paralysis of the lower limbs.
  • Inhibition of protective enzymes: Studies suggest β-ODAP can inhibit antioxidant enzymes, exacerbating cellular damage.

Understanding Neurolathyrism

Neurolathyrism is a motor neuron disease with a range of symptoms that typically progress over time. The onset can be sudden or insidious, often triggered by a period of malnutrition combined with heavy reliance on grass peas.

Symptoms often start with:

  • Muscle cramps in the calf muscles
  • Weakness and difficulty walking
  • Stiffness in the legs

As the condition progresses, it can lead to a spastic paraparesis, where an individual walks on the balls of their feet with a characteristic 'lurching scissoring' gait. In severe cases, irreversible paralysis of the legs can occur, potentially confining victims to crawling. While the primary impact is on motor function, β-ODAP may also contribute to other health issues like bone deformities in children. It is important to distinguish neurolathyrism from osteolathyrism, a connective tissue disorder caused by a different toxin found in sweet peas (Lathyrus odoratus).

Comparison of Lathyrus Toxins

Feature Neurolathyrism (Lathyrus sativus) Osteolathyrism (Lathyrus odoratus)
Toxin β-N-oxalyl-L-α,β-diaminopropionic acid (β-ODAP) β-aminopropionitrile (BAPN)
Effected Tissue Motor neurons, leading to paralysis Connective tissues (collagen), affecting bones and blood vessels
Key Symptoms Spastic paraparesis, muscle weakness, lower-limb paralysis Skeletal deformities, hernias, aortic aneurysm
Mechanism Excitotoxicity via glutamate receptors, causing motor neuron death Inhibits lysyl oxidase, disrupting collagen cross-linking

Mitigating the Risk and Modern Breeding Efforts

In communities where grass pea is an important food source, especially during times of famine, methods to reduce the β-ODAP content have been employed, though they are not always completely effective. Traditional techniques like soaking the seeds in water for an extended period and then boiling or sun-drying can help lower the toxin levels, as β-ODAP is water-soluble. However, this requires sufficient fuel and water, which may be scarce in drought-prone areas.

Agricultural research and breeding programs have made significant advances in developing new varieties of Lathyrus sativus with much lower β-ODAP concentrations. These low-toxin cultivars offer the benefits of a hardy, nutritious, and high-yielding legume without the associated health risks. This development is crucial for improving food security and public health in regions historically affected by neurolathyrism.

Conclusion

The neurotoxin β-ODAP is the primary toxic compound found in Lathyrus legumes like the grass pea, and its chronic overconsumption can lead to the crippling neurological disorder known as neurolathyrism. This condition, characterized by motor neuron degeneration and paralysis, results from the excitotoxic effects of β-ODAP on the central nervous system. While traditional processing methods exist to reduce the toxin's concentration, modern agricultural science has focused on developing genetically improved, low-toxin varieties to ensure a safer and more reliable food source for vulnerable populations. Continued research and public health education are essential for managing the risks associated with this once-feared but resilient crop.

Authoritative Reference

For more detailed scientific information on the neurotoxin and neurolathyrism, a comprehensive overview can be found in a paper published on PubMed: Lathyrus sativus (grass pea) and its neurotoxin ODAP.

Frequently Asked Questions

The neurotoxin β-ODAP is primarily associated with Lathyrus sativus, also known as grass pea, chickling pea, or khesari dal. Other species in the genus, like Lathyrus cicera and Lathyrus ochrus, also contain ODAP to a lesser extent.

The disease caused by the consumption of Lathyrus seeds containing β-ODAP is called neurolathyrism.

Early signs of neurolathyrism include muscle cramps in the legs, weakness, and difficulty walking. These symptoms can be gradual or have a sudden onset.

No, paralysis is a result of chronic exposure. Neurolathyrism develops after a prolonged period of consuming large quantities of Lathyrus seeds, not from a single ingestion.

While the entire genus should be viewed with caution, the level of neurotoxin varies by species and cultivar. For example, the garden sweet pea (Lathyrus odoratus) contains a different toxin that causes osteolathyrism, which affects connective tissues, not nerves.

Traditional methods like soaking the seeds in water and then boiling can help reduce the levels of water-soluble β-ODAP. However, these methods are not 100% effective, and the most reliable approach is to use modern, low-toxin cultivars.

Yes, through advanced breeding programs, researchers have developed varieties of Lathyrus sativus with significantly lower β-ODAP concentrations, making them safer for human consumption.

References

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Medical Disclaimer

This content is for informational purposes only and should not replace professional medical advice.