Isolation of Toxic Crystals from Sweet Peas (
            <i>Lathyrus odoratus</i>
            )

Dasler, Waldemar

doi:10.1126/science.120.3112.307

Cited by 42 publications

(20 citation statements)

References 3 publications

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“…These studies suggest a completely new approach in both the understanding and treatment of hypertension; namely, agents that interfere with deposition of vascular connective tissue. Obviously, such agents can produce toxic manifestations (6,18,19). However, it should be remembered that the lathyrism produced by (l-aminopropionitrile is a disease limited to young, rapidly growing animals, while the incidence of hypertension in man is mostly in the older population.…”

Section: Discussionmentioning

confidence: 99%

Reduction of blood pressure and vascular collagen in hypertensive rats by beta-aminopropionitrile.

Iwatsuki¹,

Cardinale²,

Spector³

et al. 1977

Proc. Natl. Acad. Sci. U.S.A.

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#-Aminopropionitrile, a specific inhibitor of lysyl oxidase preventedthe rise in blood pressure induced by deoxycorticosterone-salt in rats. In addition, after the onset of hypertension, administration of P-aminopropionitrile lowered the blood pressure. Concomitant with the lowering of blood pressure, there was a reduction in the more highly crosslinked form of vascular collagen. These findings would indicate that increases in vascular connective tissue are not only sequelae of hyprtension, but may also contribute to the maintenance of eevated blood pressure. We have previously reported that vascular collagen biosynthesis and deposition is increased in hypertensive rats and that these effects are reversed when blood pressure is lowered by antihypertensive drugs (1, 2). Those findings suggested that the deposition of vascular connective tissue is one of the sequelae of hypertension. The availability of agents that selectively inhibit collagen formation and deposition make it possible to determine whether the increased amounts of collagen also contribute to the maintained hypertension. One of these agents, fl-aminopropionitrile, is a fairly specific inhibitor of lysyl oxidase, the enzyme which catalyzes the oxidative deamination of the e-amino groups of lysine and hydroxylysine in collagen and elastin (3-5). In the absence of lysyl oxidase activity, the formation of crosslinked collagen is blocked. This can be demonstrated by a diminution of insoluble collagen (6).In the present study we have shown that administration of f3-aminopropionitrile to rats receiving deoxycorticosterone-salt markedly diminishes the hypertension produced by the steroid. Rats were killed by decapitation. The entire aorta and the mesenteric artery were excised from each animal and perivascular adipose tissue was carefully removed from them. Each vascular tissue was homogenized in 30 volumes of 0.5 M acetic acid in a ground-glass homogenizer, and the soluble collagen was extracted for 24 hr at 40 (10). The extracts were centrifuged at 11,500 X g for 30 min and the supernatants were dialyzed against 10 mM acetic acid. The precipitates, containing the insoluble collagen, were then lyophilized. After this, the supernatants and precipitates were hydrolyzed in 6 M HCl for 20 hr at 105°. Hydroxyproline was measured by the method of Kivirikko et al. (11). These values yield collagen content when multiplied by 6.98 (12).Tissue sections from each experiment were prepared for histological examination. RESULTSChanges in blood pressure and body weight As shown in Fig. 1, the blood pressures of the rats treated with deoxycorticosterone-salt were markedly increased over those of the controls. Administration of (3-aminopropionitrile to rats treated with deoxycorticosterone-salt largely prevented the increase in blood pressure for 5 weeks. After this time, the blood pressure gradually increased to about 170 mm of Hg by the fifteenth week of treatment. At this point, however, the blood pressure was still much lower than in the rats treated with de-o...

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Section: Discussionmentioning

confidence: 99%

Reduction of blood pressure and vascular collagen in hypertensive rats by beta-aminopropionitrile.

Iwatsuki¹,

Cardinale²,

Spector³

et al. 1977

Proc. Natl. Acad. Sci. U.S.A.

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“…The lathyrus activity of BAPN has also been observed independently by others (3,4). Knowing the formula of the toxic component, it seemed desirable to study further the mechanism by which BAPN exerts such a profound effect on mesenchymal tissues in growing rats.…”

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confidence: 87%

“…Even though it was not possible to inhibit periosteal fibrosis of the femur or skeletal deformity, there is a suggestion that other related changes such as herniation, paralysis, aortic rupture, weight gain, and muscle spasticity may have been affected by the supplements. For example, hernias were not observed when the diets were supplemented with methionine, or a mixture of L-arginine and L-lysine (Assays 3,9). Hind limb paralysis, secondary to marked vertebral column deformities, was most pronounced in the group which received 0.35% BAPN and 0.35% p-alanine (Assay 4).…”

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confidence: 97%

Lathyrus Factor Activity of Beta-Aminopropionitrile and Related Compounds.

Bachhuber

Lalich

Angevine

et al. 1955

Experimental Biology and Medicine

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“…The compound proved to be an osteolathyrogen, the active portion of the molecule being b-aminopropionitrile (BAPN) [Dasler, 1954]. A second compound which was acutely toxic to rats was subsequently isolated from seeds of L. latifolius and identified by Ressler et al [1964] as L-2,4-diaminobutanoic acid (DABA).…”

Section: Introductionmentioning

confidence: 99%