Comparative effect of dietary administration of Lathyrus sativus pulse on behaviour, neurotransmitter receptors and membrane permeability in rats and guinea pigs

Abstract

Neurolathyrism, an upper motor neuron disease, has been thought to be caused by long-term dietary consumption of lathyrus pulse, which contains the toxin beta-N-oxalyl-L-alpha,beta-diaminopropionic acid. Earlier behavioural studies employing oral feeding of lathyrus pulse to animals has been conducted without evaluating the biochemical toxicity potential. In the present investigation the effect of dietary feeding of 10%, 50% and 80% lathyrus pulse to rats and guinea pigs for 3 months on neurobehavioural parameters, including locomotor activity, inclined plain test and neurotoxicological parameters such as neurotransmitter receptor binding, Ca(2+) influx and membrane fluidity, was investigated. Exposure of 50% low and high toxin lathyrus to rats did not cause any significant change in locomotor activity, whereas guinea pigs at the same dosage regimen of high toxin lathyrus showed significant lowering of inclined plain test scores. Furthermore, studies of neuroreceptor binding in rats fed 50% low and high toxin lathyrus showed significant changes in glutamate, dopamine and muscarinic receptors, whereas the benzodiazepine receptor elicited no change. Guinea pigs, on the other hand, fed 50% and 80% lathyrus in the diet showed significant changes in glutamate, dopamine, muscarinic and benzodiazepine receptors. Interestingly, significant elevation in intracellular calcium with a concomitant increase in membrane fluidity was observed in rats (50% low and high toxin) and guinea pigs (50% and 80%) fed a lathyrus diet. These results indicate that although both species (rats and guinea pigs) are susceptible to neurochemical changes on exposure to lathyrus, locomotor changes are only noticed in guinea pigs. Thus, guinea pigs may be more prone to lathyrus toxicity and may serve as a sensitive animal model compared with rats.

Potentiation of neurotoxicity ofLathyrus sativusby manganese: Alterations in blood–brain barrier permeability

“…Although the nonprotein amino acid, -ODAP (-N-oxalyl-L-, -diamino propionic acid), present in grass pea was identified as the causative agent some four decades ago (Murti et al 1964;Rao et al 1964), the precise role of ODAP and its mechanism of action vis-à-vis human lathyrism still remains unclear (Yan et al 2006). Several risk factors and pre-disposing conditions such as malnourishment, genetic susceptibility, altered blood-brain barrier permeability, and trace metal imbalance have been claimed to increase the neurotoxicity of grass pea (Jahan and Ahmed 1993;Lambein et al 1994;Lambein and Kuo 1997;Mishra 1999;Banga 2001;Amba et al 2002a;Kumar et al 2003).…”

The influence of Chakawar (Cassia tora) and Khesari (Lathyrus sativa) seeds on the growth and biochemical performance in the blood of albino rats

“…It can be used as a green fodder while seeds can be used for feeding of the animals. The major limitation to its use is the occurrence of toxin BOAA (B-n-oxalyl-amino alanine) which may cause neurolathyrism in human consumption (Amba et al, 2002 andRudra et al, 2004). Lathyrism develops only when the consumption of seed is high (300 g daily) and it is used for a period of more than six months (Manay et al, 2008).…”