506 G. H. BERGOLD 



larvae (Yamafuji et al., 1954). No difference between the oxygen consumption 

 of dissected tissue of infected and healthy B. mori larvae was found by 

 Gratia et al. (1945), but Akune (1951a) observed an increase in the respiratory 

 and a decrease of the catalase activity. Similarly Gershenson (1956a) found a 

 higher O.^ concsntration in infected Antherea pernyi Guer. pupae, which, how- 

 ever, decreased at the time of death to the level of healthy pupae. Ishimori 

 and Osawa (1951) found, after an initial drop, a rapid increase of the catalase 

 activity upon appearance of polyhedra in the blood cells. The inhibition 

 of endogenous respiration of a homogenate of B. mori larvae infected with 

 cytoplasmic polyhedrosis by 0.01 M EDTA is less than in healthy larvae but 

 can be restored by the addition of Mg++, Mn++, Co++, and Fe+++, but not 

 with Cii++. The rate of recovery is greater in diseased than in healthy larvae, 

 but no difference was found in the activities of cytochrome oxidase and 

 succinic dehydrogenase in mitochondria. In homogenate and mitochondria 

 the oxidation of succinate, malate, and glutamate was decreased in the 

 diseased larvae, and in mitochondria the activity of glutamate oxidation by 

 DPN and succinate oxidation by ATP was also less in diseased than in healthy 

 larvae (Ishikawa, 1958). The hexokinase activity on glucose and fructose 

 in the fat body of B. tnori larvae appears to be decreased at the onset of 

 symptoms of polyhedrosis (Shigematsu, 1958), but the dehydrogenase 

 activity in larval blood and pupal homogenate is increased in diseased B. 

 mori (Murai and Aizawa, 1957). 



Investigations of the amino acid metabolism revealed that there were no 

 changes in the hemolymph of infected B. mori larvae until the disease had 

 well progressed (Drilhon 1951; Drillion et al., 1951, 1952). However, an increase 

 in histidine and a decrease in aspartic acid, cysteine, glutamic acid, glutamine, 

 threonine, tyrosine, and valine were observed in another investigation 

 (Ishimori and Muto, 1951). Alkaline extraction (0.05 N NaOH) of diseased 

 and healthy B. mori larvae with acetone show no difference (Yoshihara, 

 1952). The activity of a dipeptidase and of a peptone-decomposing enzyme 

 appears to be increased (Yoshihara 1956a,b), as weU as that of a trans- 

 oximase, which could also be boosted by feeding NaNOg, KNO2, and 

 (NH4)2C03 (Yamafuji et al., 1953b). The KgO content of diseased B. mori 

 larvae appears to be decreased (Alcmie, 1951b). Feeding B. mori larvae 

 with young mulberry leaves leads to a rise in the acidity of body fluids 

 (over 300 mg. % of ammonium N in excreta), which provokes polyhedrosis. 

 Insufficient amomits of K in the oak leaves favors the outbreak of poly- 

 hedrosis in A. pernyi larvae (Arseniev and Bromley, 1951). The addition of 

 cobalt nitrate and cobalt sulfate (0.05 %) to the food of B. mori larvae 

 decreases frequency of " spontaneous " polyhedrosis, particularly if Ca 

 CI2 (1 %) is added (Gershenson, 1958). 



The concentration of protem is higher (5.4 %) in diseased larvae than in 



