Commentary on a review on the mechanism of Ackee-induced vomiting sickness

A recent review article concluded that glutamic acid probable plays a central role in the vomiting and neurological features of ackee poisoning. The present article draws attention to misconceptions in the basis of that hypothesis, and reviews important evidence suppporting a different role (AU)

A re-examination of the mechanism of ackee-induced vomiting sickness

The hypoglycemia seen in ackee poisoning almost certainly results from the presence of hypoglycin A in the aril. However, the mechanism underlying the vomiting and neurologic disorders have not been properly established. We have, in this review, re-established the latter and proposed that the vomiting and neurological features of ackee poisoning probably result from the excitotoxic properties of glutamic and aspartic acids derived directly and indirectly from ackee intake (AU)

[15N]Glycine metabolism in normal man: the metabolic O-amino-nitrogen pool

[15N]Glycine was infused into fed, fasted or acidotic humans. In all metabolic states there was considerable transfer of labelled nitrogen to urea and amonia, but alanine and glutamate did not become enriched. The findings show that free exchange of nitrogen between all amino acids does not take place. Glycine, serine, threonine, lysine and histidine cannot be considered part of the a-amino-nitrogen pool as classically conceived, although they form up to one-half of that pool. (AU)

Monosodium glutamate in the chick embryo: lack of obvious toxic or teratogenic effects when administered at 24 hours incubation

The administration of monosodium glutamate (MSC) to chick embryos at 24 hours did neither produce gross developmental defects nor influence growth by 72 hours total incubation. The concentration of MSG administered ranged from 0.3 to 46.6 percent, the volumes injected being 0.05, 0.1, or 0.2 ml. Several injection methods were evaluated. It is suggested that injection into the centre of the yolk is the most effective way to give water-soluble treatments during this period of development (AU).

Haemoglobin Spanish Town alpha27 Glu replaced by Val (B8)

A new alpha chain variant Hb Spanish Town, a27 Glutamic acid-Valine, awas detected in the cord blood of a Jamaica Negro infant. In the mother the adult component (a2 Spanish TownB2) has an electrophoretic mobility between haemoglobins S and F at alkaline pH and measures 11.0-12.0 percent of the total haemoglobin. (Summary)

Control of renal cortex ammoniagenesis and its relationship to renal cortex gluconeogenesis

The metabolism of glutamate by kidney cortical slices from normal and acutely acidotic rats and the effect of acidosis in vitro on the metabolism of these two substrates has been investigated. The effects of calcium on all these processes was also studied. Kidney cortical slices from acutely acidotic rats utilized more glutamine and formed more ammonia, glucose and glutamate than slices from rats. Increased glutamine utilization and ammoniagenesis by cortical slices from acidotic rats was not detected when Ca2+ was omitted from the medium, although glucose formation was still enhanced and glutamate formation decreased. With in vitro acidosis there was no change in glutamine uptake in the presence or absence of calcium but with calcium, ammonia production fell. Although there was no change in glutamate uptake by cortical slices from acidotic rats, there was an increase in ammoniagenesis and gluconeogenesis with or without calcium. With in vitro acidosis the only significant changes were an increase in ammoniagenesis and gluconeogenesis in the absence of calcium. The results show that ammoniagenesis from glutamine is controled by a rate-limiting step distinct from that which controls deamination of glutamate and gluconeogenesis from glutamine and glutamate. Possible control points and the interrelationship between ammoniagenesis and gluconeogenesis are discussed (AU)

The effect of phenyl ethyl biguanide in vivo and in vitro on gluconeogenesis and ammonia production in rats

The drug phenyl ethyl biguanide (PEBG) was used in vivo and in vitro to study further the relationship between renal gluconeogenesis and ammonia production in the rat. When PEBG was injected intraperitoneally into the rats, it caused a decrease in urinary ammonia in spite of a greater degree of systemic acidosis. PEBG injections also blocked the increase in glucose and ammonia production by renal cortical slices from rats which had been made acidotic by oral administration of ammonium chloride 2h previously. With increasing concentrations of PEBG in vitro, there was inhibition of gluconeogenesis and ammonia production from glutamine and glutamate as substrates. The two processes were equally inhibited when glutamate was used as substrate but with glutamine, gluconeogenesis was more inhiblted than ammonia production. The inhibition of renal gluconeogenesis by PEBG in vitro was similar when succinate, oxaloacetate, fructose, glutamine and glutamate were used as substrates. The results show that PEBG does not inhibit gluconeogenesis by blocking a specific site in the gluconeogenic pathway. In addition, further proof is provided of the physiological interrelationship of renal ammonia production and gluconeogenesis (Summary)

Protein turnover in skeletal muscle. I. The measurement of rates of synthesis and catabolism of skeletal muscle protein using [14C]Na2CO3 to label proteins

The turnover of rat skeletal muscle protein was studied using [75Se]selenomethionine, [6-14C]arginine and [14C]Na2CO3 to label protein. In rats labelled with both [75Se]selonomethionine and [14C]Na2CO3 the 14C activity of mixed skeletal muscle protein fell rapidly with a half-life of 6.0 days for the specific activity and 10.5 days for the total activity. There was no loss of 75Se activity from muscle protein during the 12 days of the experiment. Following the injection of [6-14C]arginine both sarcoplasmic and myofibrillar proteins continued to incorporate label for 6 days after which time the label was lost fairly rapidly. Following injection of [14C]Na2CO3 muscle protein was maximally labelled by 6h, at which time specific activity of the free amino acids had fallen to a very low level. Aspartate and glutamate in particular had lost over 99 percent of their maximum activity by this time in comparison to arginine which was still highly labelled after 24h. 14C activity was lost more rapidly from aspartate and glutamate isolated from sarcoplasmic and myofibrillar protein than from other labelled amino acids. The half-lives of the two protein fractions were 3.9 and 7.2 days from the specific activity curves and 6.0 and 19.0 days from the total activity curves. The differences between the half lives of muscle proteins labelled with amino acids are discussed in terms of the effects of reutilization of the labelled amino acids used. It is postulated that aspartate and glutamate labelled by the injection [14C]CO3= are only reutilized to a very small extent and therefore afford the means by which the rates of protein synthesis and catabolism in skeletal muscle can be measured with reasonable accuracy (Summary)