일산화탄소 중독가토 조직내의 lactic dehydrognease 활성의 변화에 관한 연구

Abstract

[한글]

[영문]

To study the CO intoxication upon protein and upon lactic dehydrogenase activity and its isozymes, homogenates of brain, liver, and skeletal muscle were examined in the following groups of experimental animals.

1. Chronic CO exposure group: Twenty four marc rabbits were exposed to 90 to 115ppm(average 100ppm) of CO for 8 hours per day for 9 days.

2. Acute CO intoxication group : Six male rabbits were exposed to 7,000 ppm of CO for eight tours.

3. Group treated to low oxygen pressure: Six marc rabbits were treated on talc low atmospheric pressure equivalent to 18,700 ft. attitude for eight hours.

In addition to the above investigation in vivo, the direct effects of CO on the enzymatic system was also studied by the determination of the lactic dehydrogenase activity with the enzyme and NAD co-enzyme, preliminary treated by CO in vitro. The

results an as follows:

1. The weight of the liver per unit body weight of the rabbit was gradually decreased up to six-th day and recovered after following three days. On the contrary, the proportional weight of the kidney of the animal on chronic exposure was increased.

2. The activity of lactic dehydrogenase was decreased from third day and almost recovered at ninth day. The lowest activity was shown on talc sixth day of chronic CO exposure. CO sensitivity, as demonstrated by enzyme activity, was decreasingly

higher in kidney, brain, heart.

3. In talc patterns of M and H isozyme of lactic dehydrogenase of the heart and kidney, the normally dominating bands were decreased in CO exposure.

4. The activity of lactic dehydrogenase was remarkably decreased in heart, brain and kidney follow-ing acute CO intoxication with anoxia, however, this did not occur with simple hypoxia.

5. In the alteration of organ cells, damage to mitochondria was observed in the liver, kidney and heart, decreasingly, by talc electron microscopy, and was correlated to the alteration of lactic dehydrogenase.

6. When NAD, co-enzyme, previously treated by CO was used in talc enzymatic reaction in vitro, NADH was not produced even though sufficient lactic dehydrogenase and lactate as substrate, were added in vitro.

Therefore, it is considered that the anoxia and alteration of lactic dehydrogenase in the tissue following the inactivation of co-enzyme by CO an the causes of CO-intoxication.