???(diallyl disulfide)? ??? A(retinal acetate)? ??? ?? ??? ??? ??

? ??? ʳƷ�l��? �h���l��? ?? Σ������?? ??? ???? ??? ????? ????? ?? ????? ??? A? ??? Σ�� ?? ?? ????? ????, ???��¶? ?? ����ˮ��? ����??? HSP(Heat Shock Protein, ���n�������| ?? ????�����|)? �l�@�r��? �l�@�̶�? ????? ?????. ?????? Wistar? SPF ?? ?? 483??? ??????, ����Ⱥ, ???Ͷ�cȺ(Cd, CdCl?20 �J/�K), ???? ??? (diallyl disulfide) Ͷ�cȺ(Cd+Dds, diallyl disulfide 50 �J/�K), ???? ??? A(retinol acetate) Ͷ�cȺ(Cd+Ra, retinol acetate 50,000 I.U./�K)?? ?????. ????? ?? ??? ?? 1, 2, 4, 8, 16, 24??, 2, 4. 7?, 2, 4, 8, 16?? Ͷ�c????, ??? ??? ??? ??. 1. ???Ͷ�c �� 4??? Ѫ�� ???����? 0.972��l.256 ?/g?? ����Ⱥ? 0.004?/g? ??? ?????, Ͷ�c 2???? ���K? ???����? 23.76��24.84 ?/g?? �I�K? 20.53��22.03 ?/g?? ????, 8? ???? ���K? ???����(82.48��86.37 ?/g)?? �I�K? ???����(98.0��109.8 ?/g)? ? ???. ???, ???? Ͷ�c �� 4??? ?? ?? ?? ????, ?? ���K?? ???? ?? ���K?? �I�K?? ??????, 8? ???? ���K?? �I�K? ??? ��e��? ???? ??? ????. 2. ???Ͷ�c? ?? Ѫ�[?? ���� ׃��?? ALT(Alanine Aminotransferase), AST(Aspartate Aminotransferase) ���Զ�? Ͷ�c �� 1???? ?? 60.3��73.0 U/?, 135.5��149.8 U/?? ????? ���K ����? ???? ??? ?????, glucose? Ͷ�c 8?? ����Ⱥ(113.8 �J/?)? ??? Cd+RaȺ? ??? ?? Ⱥ?? 72.8��77.5 �J/?? ?? ??? ?? ???? ????? ???? ������(p<0.05)? ???. BUN(blood urea nitrogen)? Ͷ�c 4?? ����Ⱥ? 19.3 �J/?? ??? Cd, Cd+DdsȺ?? 24.8��25.8 �J/? ����? ??? ????, Cd+RaȺ??? Ͷ�c 16??, CdȺ? 33.2 �J/?? ??? 27.3 �J/??? ����??(p<0.05) ???. Creatinine? ?? ԇ�Ⱥ?? Ͷ�c 8?? ����Ⱥ? 0.77 �J/?? ??? 0.98��1.38 �J/?? ?? ??? ????(p<0.05), 16??? CdȺ? 1.20 �J/?? ??? Cd+RaȺ? 1.02 �J/?? ����?? ?? ??? ???(p<0.05). 3. �����M���W? �z�� ?? CdȺ? Cd+RaȺ??? Ͷ�c 8??? �I�K�����? ��ǻ? �������w��?? ��A��(urinary cast)? ??????, Cd+DdsȺ? �I�K ��λ����� ��Ƥ����? �@��? ׃������? ????. ??��? ???Ͷ�c 8??? ������(seminiferous tubule) ??? �g�|�M��? ������ Һ�w? �A��? ?? ???? ??? ������? ??? ή�s?? ?? ??? ???. Cd+DdsȺ? Cd+RaȺ??? CdȺ?? ��׃? ΢��???. ???? 2??? Ͷ�c? ???? �I�K? ����@΢�R ��Ҋ? ��λ������� ����? �����| �[Û, ??????? ׃��, �����| С��? ??, ë��Ѫ�� ��Ƥ����? �����| �[Û? �ճh�γ�?? ???? ??????, Ͷ�c 8?? ??? �I�K����� ��ǻ? �o���| С��? ??? ׃�� ��Ƥ����? ??? ?????. 4. HSP_(70)? ???Ͷ�c �� 2???? �l�@? ????, 48???? ���m??, ??? ԭ��B? �֏�?? ??? ????. ???? HSP_(70)? �l�@? diallyl disulfide? retinol acetate Ͷ�c? ?? ??? ?? ???. �I�K??? HSP_(70) �l�@? �z���w? �������Ƥ����?? ?? �l�@?? ??? ????. ??? ?????, ??? ???? Ͷ�c??? ? HSP_(70) �l�@? Ͷ�c �� 2��4?? ?? ???? Ѹ��? ����?? ? ? ???, ???(diallyl disulfide) Ͷ�c? ???? ?? �I�K�p��? ���M???, ??? A(retinol acetate) Ͷ�c? ???? ?? �I�K�p��? ����??? ??? ???. ???? ?? ??��??? ???(diallyl disulfide) ?? ??? A(retinol acetate)? Ͷ�c???? �p�� ���RЧ��? ???.

Department of Environmental Health, Yongin University, Yongin city, 449-71 4 ABSTRACT-Garlic occupies a special position among the many foods of vegetable origin be- cause it is the sole food for Koreans during the their lives. And vitamin A has been ingested by forms of food or additives. Cadmium has been described as 'one of the most dangerous trace ele- ments in the food and environment of man and livestocks'. Since the de novo synthesis of stress proteins can be detected early after exposure to some agents, analysis of cadmium-induced changes in gene expression, i.e. alterations in patterns of protein synthesis, may be useful to de- velop as biomarkers of exposure and damage for food hygiene. The acute and chronic combined ef- fects of cadmium (Cd, CdC1, 20 mg/kg), garlic oil (Dds : diallyl disulfide 50 mgkg, 3 times a week) and vitamin A (Ra : retinol acetate 50,000 IUkg, 3 times a week) on Wistar male rats were evalu- ated concerning cadmium contents, tissues enzyme activity, HSP expression, histopathological and electron microscopical examinations. The results of the study are as follows : 1. Less cad- mium was absorbed through the digestive tracts, but the ratio of contents in renal to hepatic cad- mium was higher at 8 weeks after treatment. The cadmiun contents in tissue were not changed by the simultaneous administration of diallyl disufide or retinol acetate. 2. ALT (alanine am- inotransferase), AST (aspartate aminotransferase), glucose, BUN (blood urea nitrogen), creatinine, the key indices of the clinical changes in hepatic and renal function were significantly changed by the cadmium treatment after 1 week in liver, after 4 weeks in kidney. 3. Histopathological changes in cadmium treated rats were appeared at 8 weeks after treatment in ludneys. Homo- genous eosinophilic material was accumulated in cortical and collecting tubular lumens at 16 weeks. Degenerated or necrotized tubular cells were observed in cortex and medulla. Degenerated seminiferous tubules and homogeneous eosinophilic material was seen in interstitial tissue of rat treated with cadmium for 16 weeks. Calcium deposits were seen in degenerated seminiferous tu- bules and the tubules showed severe calcification of rat treated with cadmium for 16 weeks. Elec- tron microscopic changes in kidney were observed in rats treated with CdC1, 20 mgkg. Proximal convoluted tubule cells showed swelling of cytoplasm and narrow lumen. Capillary endothelial cells showed cytoplasmic vacuoles and swelling. Degenerated epithelial cells were accumulated in tubular lumen of kidney. 4. Enhanced synthesis of 70 KDa relative molecular mass proteins were detected in 2 hours after cadmium exposure, with maximum activity occurring at 8-48 hours. In- duction of HSP 70 was evident at proximal tubules and glomeruli in kidney. Testicular cells pro- duced enough HSP to be detected normally. From the above results, it could be concluded that HSP,, induction by the cadmium treatment was a rapid reaction to indicate the exposure of xe- nobiotics, and retinol acetate reduced the cadmium induced nephrotoxicity. Key words cadmium, HSP70, diallyl disulfide, retinol acetate