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Report describing a zero-power reactor facility (ZPR-VII), its systems, and associated hazards.

Drosophila melanogaster larvae require choline for growth but when fed dl-carnitine in place of choline, carnitine is decarboxylated to β-methylcholine and phosphatidyl-β-methylcholine is synthesized to replace phosphatidylcholine. Feeding (−)-carnitine in place of choline results in a moderate deficiency of lecithin-type phospholipid and a corresponding reduction in growth. The capacity of larvae to employ (+)-carnitine for phosphatidyl-β-methylcholine synthesis and subsequently for growth is very limited. Only 41% as much phosphatidyl-β-methylcholine is synthesized by larvae fed 5.7 X 10−4 M (+)-carnitine as is formed when the same concentration of (−)-carnitine is fed. This suggests that (−)-carnitine is the preferred substrate for carnitine decarboxylase, the enzyme that degrades carnitine to form β-methylcholine. Utilization of carnitine for phospholipid synthesis is clearly dependent upon a choline-deficient state. The presence of small quantities of choline, either in body tissues or in the diet, inhibits the incorporation of carnitine derivatives into phospholipid. Intact carnitine is needed for maximum larval growth and adult activity, indicating that D. melanogaster larvae synthesize a suboptimal quantity of carnitine. Thus, dietary carnitine supplements in vivo carnitine synthesis for physiological purposes.