간디스토마 감염가토(感染家兎)의 Vitamin A 부하(負荷)에 관한 연구

Abstract

Clonorchis sinensis principally lives in the bile bucts absorbing nutritional

substances and leading to chronic peribiliary inflammation due to mechanical

irritation. During infection of Clonorchis sinensis, nightblindness frequently

appears due to deficiency of vitamin A (vit. A). Levine (1958) observed one case of

nightblindness in the experimental infection of Amphimerus pseudofelineus of cat.

However, Bercovitz(1931) reported previously the symptom could disappear on

inducing the excretion of bile from the duct.

Lewis(1942) observed that the serum vit. A decreased when residual vit. A in the

liver tissue was exhausted. Kim (1964), recently, reported that vit. A loading in

infected animal caused the temporary raising of serum value.

The object of the present study is to confirm the fate of vit. A which was

absorbed from the intestinal wall of the rabbit infected with Clonorchis sinensis

and to clarify the mechanism of the vit. A deficiency.

Materials and Methods

Animals: White rabbits(1.6∼2.0kg) were used as experimental animals and were fed

similarly.

Metacercariae: Metacercariae of Clonorchis sinensis were collected by digestion

method from fresh water fish caught from an endemic area (Iri Chollabuk-Do).

About 1,500 of the larvae were given orally, and 6 weeks after the infection

egg-out-put was confirmed by stool examination.

Vitamin A: Water soluble(U.S. vitamin corportion). For loading 15,000㎍ of vit. A

was given orally and 3,000 ㎍ intravenously.

In order to calculate the vit. A, Georgy modification of Dann & Evelyn method was

applied for serum vit. A, and Oser, Melnick Pader's method for tissue vit. A. 3∼4

gm of liver tissue weighed and sliced into small pieces and followed by the regular

procedure. A number of Clonorchis sinensis from the bile duct were washed with

saline several times and followed the same procedure. Vit. A in bile juice and

urine was measured by the same method, except replacing the 0.5 N alcoholic

potassium hydroxide into 95% ethyl alcohol in order to coagulate the protein

substances.

Blood was taken from the heart at hunger condition at intervals of two hours in

the first part and three hours in the second part(13 hours after the vit. A was

given). the separated serum was kept at freezing temperature.

Results

The average serum vit. A in healthy rabbits was 71.1㎍% and infected group was

30.8 ㎍% 7 weeks after the infection.

When vit. A was given to non-infected group (15,000㎍), the serum value increased

to high level(198.1, 264.6, 222.4 ㎍%) from 7 to 16 hours. the decrease started

after 19 hours and recovered to original lvel after 25 hours.

In the infected group, though there were individual differences, the value of

vit. A in the serum increased to high level (296.8, 351.3, 320.7 ㎍%) from 7 to 16

hours after the administration of vit. A and showed acute decrease at 19 hours to

160.6㎍%, but still held high titre, 85.9 ㎍% even 25 hours after the loading.

In general, there was no difference of the ability of vit. A absorption between

the infected and non-infected group, but the value of vit. A in the serum after the

loading was much higher in the infected group than in non-infected.

The amount of vit. A in liver parenchyma was also calculated before and after

vit. A was given. In the infected rabbits, the weight of the liver parenchyma

increased to about 1.6 times as in the normal rabbit due to dilatation, rupture of

the capillary bile ducts, necrosis of liver parenchyma and degeneration of the

cells. However the amount of vit. A in the liver parenchyma was 61.84 ㎍/gm in the

normal group and only 13.82㎍/gm in infected group. 7 hours after vit. A was given

in the normal group the amount increased to about 1.7 times (104.53㎍/gm), but in

infected group there were no differences comparing the value before the loading,

16.56 ㎍/gm after 3 hours, 12.81 ㎍/gm after 7 hours.

In order to clarify the reason of the low value of vit. A in the liver parenchyma

of infected group, whether it was due to the loss of vit. A by means of bile juice

or consumption by the liver fluke itself, the bile juice and parasites were

examined.

Bile juice was taken from common duct hourly(normal rabbit 13 ml, moderatry

infected rabbit 9 ml, heavily infected rabbit 3 ml), but no vit. A was detected

even from the vit. A loaded group and the vit. A could not be found from the

parasite itself collected from biliary ducts numbering 600 and 1,800.

Since the storing ability of liver parenchyma in the infected group was lower

than in the normal group, the process of the rapid decrease along with time elapes

was one of the subjects to be clarified.

The amount of vit. A in kidney tissue, urine, and feces were measured comparing

the normal group. Since it took much time to get sufficient amount of stool from

the rabbit, the animals were sacrificed after a certain given time, and stool was

taken from the lower colon.

In the kidney a slight amount of vit. A was detected, bud there was no difference

between the normal and infected group. 36 hours after the vit. A loading, the

amount of vit. A in urine of normal rabbits were 22.7 ㎍ in average, whereas it was

82.7 ㎍ in the infected group. The data shows that loss of vit. A from urine in the

infected group is about 4 times that of the normal group.

The amount of vit. A in feces showed no difference between the two groups. It is

presumed a considerable amount of vit. A is excreted without absorption from the

small intestine.

Conclusion

In conclusion, it is considered that the reason of vit. A deficiency in the

infection of Clonorchis sinensis is due to the decrease of storing ability of the

liver and rapid excretion from kidney, and not by the absorbability of vit. A form

the intestinal wall.