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Cyclopiazonic acid 및 aflatoxin B<sub>1</sub>이 토끼의 혈소판 응집 및 ATP 방출에 미치는 영향
홍충만,조명행,Hong, Choong-man,Cho, Myung-haing 대한수의학회 1996 大韓獸醫學會誌 Vol.36 No.4
Cyclopiazonic acid(CPA) known as stimulating the release of intracellular calcium, aflatoxin $B_1(AFB_1)$ causing gastrointestinal hemorrhage frequently were used as model toxic mycotoxins in these studies. First of all, the effects of various mycotoxins on the platelet aggregation response were determined. The effects of mycotoxins on the ATP release from platelet by aggregating factors were investigated. The results and conclusions obtained from these studies are : 1) CPA promoted ADP, collagen, thrombin, A.A. and PAF-induced rabbit platelet aggregation. $AFB_1$ inhibited collagen, A.A. and PAF-induced rabbit platelet aggregation only. 2) CPA increased both aggregation and disaggregation time, whereas $AFB_1$ decreased in a dose dependent manner. 3) CPA increased ADP, thrombin, A.A. and PAF-induced ATP release. $AFB_1$ increased A.A.-induced ATP release and decreased PAF-induced release in a dose dependent manner. In conclusion, CPA promoted platelet aggregation by the increase of ATP. Antiaggregating effects of AFB1 may be due to decreases of ATP. These data provide the basis for the future study of roles of ATP release in platelet aggregation.
랫트의 신장 근위곡세뇨관 현탁액을 이용한 Cephaloridine의 신장독성 평가
홍충만,장동덕,신동환,최진영,조재천,이문한 한국독성학회 1995 Toxicological Research Vol.11 No.1
Rat renal proximal tubule suspension was prepared from adult male Sprague Dawley rat (250-300g) by mechanical (non-enzymatical) method and evaluated as a pontential model for mechanistic studies and early screening of nephrotoxicity, using anionic antibiotics (cephaloridine). Cephaloridine (CPL) produced an increase in LDH release into media. This release results from decrease a proximal tubule cell viability and subsequently increase the permeability of cell viability and subsequently increase the permeability of cell membrane. Since loss of intracellular potassium and ATP into media is the sign of disruption of cell membrane, especially basolateral membrane (BLM), CPL induced proximal tubule cell compromise also appear be associated with BLM, maybe $Na^+-K^+$ ATPase. Also seen was significant depression in brush border membrane (BBM) ALP activity and no significantly increase in BBM GGT activities. The inhibition of typical anion, PAH accumulation (especially, CPL 5 mM) and cation, TEA (especially, 4hours incubation) were seen dose dependently. This is because of CPL accumulation in renal proximal tubule and increase of cytotoxicity.
Cyclopiazonic acid 및 aflatoxin B<sub>1</sub>이 토끼의 혈소판에서 arachidonic acid 대사, 칼슘 동원 및 초미세구조에 미치는 영향
홍충만,장동덕,조명행,Hong, Choong-man,Jang, Dong-deuk,Cho, Myung-haing 대한수의학회 1996 大韓獸醫學會誌 Vol.36 No.4
For better understanding the interrelationship of hemorrhage and aggregation mechanism, cyclopiazonic acid(CPA) known as promoting the aggregation of platelet, aflatoxin $B_1(AFB_1)$ inhibiting platelet aggregation were used as toxic mycotoxins in these studies. In order to investigate the potential role of prostaglandin metabolism on the platelet aggregation, a variety of prostaglandin metabolites such as $PGF_{2{\alpha}}$, $PGE_2$ and $TXB_2$ were measured in homogenized rabbit platelets by TLC and LSC. And the role of $Ca^{{+}{+}}$ on the platelet aggregation was investigated by flow cytometer. Finally, the morphological effects of mycotoxins on platelet were determined by transmission electron microscope. The results and conclusions obtained from these studies are: 1) CPA induced no changes but $AFB_1$ increased $PGE_2$ and $TXB_2$. 2) CPA promoted ADP, collagen, thrombin, A.A., and PAF-induced $Ca^{{+}{+}}$ release. $AFB_1$, however, decreased $Ca^{{+}{+}}$ level except collagen-induced $Ca^{{+}{+}}$ release. When the calcium blocker, verapamil, was used, CPA decreased thrombin-induced $Ca^{{+}{+}}$ release and increased collagen, ADP, PAF and A.A.-induced $Ca^{{+}{+}}$ release. $AFB_1$ in contrast decreased the all factors induced $Ca^{{+}{+}}$ release. 3) $AFB_1$ did not induce any ultrastructural changes except large vacuole formation in a few platelets. And CPA also did not induce any changes except moderate shape change, indicator of platelet activation. In conclusion, CPA promoted platelet aggregation by the increases of $Ca^{{+}{+}}$ release but had no changes in A.A. metabolites. Antiaggregating effects of $AFB_1$ may be due to decreases of $Ca^{{+}{+}}$ release and increases of $PGE_2$ and $PGF_{2{\alpha}}$ formation. These data provide the basis for the future study of mobilization and function of $Ca^{{+}{+}}$ in platelet aggregation.
Sambutoxin이 토끼의 혈소판 응집에 미치는 영향
홍충만,조명행,Hong, Choong-Man,Cho, Myung-Haeng 한국독성학회 1998 Toxicological Research Vol.14 No.3
Sambutoxin, a newly purified mycotoxin in Koea, caused hemorrhage in the stomach and intestine of rats. To elucidate the mechanism of hemorrhage, effects of sambutoxin on rabbit platelet aggregation were investigated. First of all, the effects of sambutoxin on the platelet aggregation response and ATP release from platelet by various appregating factors were investigated. And then the role of $Ca^{2+}$ on the platelet aggregation was investigated by flow cytometer. Finally, morphological effect of sambutoxin on platelet ultrastructure was examined by transmission electron microscope. Sambutoxin inhibited aggregation induced by ADP, collagen, thrombin, and arachidonic acid and decreased platelet activating factor-induced disaggregation time in a dose dependent manner. Sambutoxin also decreased thrombin and arachidonic acid-induced ATP release, but increased all factors induced $Ca^{2+}$ release. Sambutoxin showed severe ultrastructural changes of platelet such as appearance of disorganization debri of cellular organelle in intercellular space. Our results indicate that sambutoxin inhibitis rabbit platelet aggregation, and it may be party due to the decrease of ATP release. However, it is not clear whether the antiaggregating effect of sambutoxin is related to $Ca^{2+}$ increase.
홍충만,신동환,이원규,윤창용,장동덕,조재천,원도희,최광식 식품의약품안전청 1998 식품의약품안전청 연보 Vol.2 No.-
철분을 자량급여하여 간세포에 칭착할 때 발생하는 지방과산화는 찰분이 촉매역할을 하며, rnnlondialdehyde(HDA)와 4-hrdroxynonenal(4-HNE)와 같은 알데허드를 형성한다. 그리고 지방과산화는 간세포외 손상, 섬유화,경화 심한 경우 간암과도 관련이 있는 것으로 알려져 있다. 본 실험의 목적은 참깨 기름의 한가지 성분으로 항산화제인 sesamol이 carbonyl iron으로 유발한 지방과산에 미치는 영향을 알아보는 것이다. 실험동물은 수컷 SD 랫드를 사용하여 I군은 정상사료, ll군은 3.0%의 carbonyl iron 첨가사료, 111군은 0.5% sesamol 첨가사료 그리고 IV군 은 3-0%의 carboayl iron과 0.5% sesamol 동시에 첨가된 사료를 'S주와 12주 동안 급따하였다. 철분을 over-loading한 실험군에서 체중 감소와 함께 간의 상대중량이 증가하였으며, sesamol을 더욱 체중을 감소Al켰고 간웨 상대중량도 철분투여군보다 증가하였다. 그리고 alanine aminotransferase(ALT), asparto arninotransferase(AST) and gainrna glutauiyl transpeptidase(GGT)의 활성도가 철분을 32주 동안 투여한 군페서 유의하게 증가하였지만 sesamol은 이런 』ㄴLT와 AST 변화를 강소륵키지 못하였고 GGT의 경우 더욱 증가시켰다. 그러나 혈청 lactic dehydrogenase(LlIH), 알뿌민,콩단백질, alkaline phosphatase(ALP) 및 간 균질꺽의 glutathione(GSHI는 간 실험군과 유의한 변화가 관찰되지 않았다. 간 균질액의 sufleroxide dismuso(SOD)는 철분을 급여한 실험군에서 유의성있게 감소하였으며 sesainol의 동시 급여도 6주에는 치것을 증가시키지는 못하였으며, 12주에는 오 . 궤려 SOD를 감소시켰다. 이런 결과를 통하여 철분에 의하여 유발된 지방과산화가 sesamol의 동시급여에 의괘서 더욱 오허려 촉진되는 일부 결과를 관찰찰 수 있었다. 앞으로 이런 일부의 실험 결과를 화인하기위하여 다양한 실험방법을 통한 계속적인 지방과산화 연구를 수행해야 할 것이다. 향후 이런 연구는 지방과산화 모델을 퉁한 다른 식품 중의 항산화제의 :역할을 규명하는데 중요한 역할을 할 수 있을 것이다. f In hepatic iron overload, iron-catalyzed lipid peroxidation has been implicated in the mechanisms of formation of aldehyde products such as malondi.aldehyde(MDA) and 4-hydroxynonenal(4-HNE), hepatocellular injury, and fibrosis. The effect of dietary sesamol supplernentation on carbonyliron-indueed lipid peroxidation was studied. Male SD rats were fed diets supplemented with 3.0% car-boByl iron and/or 0.5% sesaHol for 6 weeks and 12 weeks. IrolR overloading resulted in significant de-creases in body weights and increases in liver to body weights ratio, which were aggravated by sesamotsupplementation. Alanine aminotransferase(ALT), aspartate aminotransferase(AST ) and r-glutamyltranspeptidase(GGT) activities were significantly increased by iron overloaded serum ; suppleraentationwith sesamol did not reduced ALT and AST levels, and more increased GGT level at 12 weeks followingtreatment. And there were no significant differences in lactic dehydrogenase(LDH ), albumin, total pro-tein and alkaline phosphatase(ALP) activities in serum, and gllltathione(GSH) in liver homogenate. Su-peroxide dismutase(SOD) in liver homogenate were significantly decreased by iron overloaded serum ;sopplernentatioB with sesa:not did not increased SOD levels at 6, weeks, and more decreased at 12 weeks.These resutts suggest that lipid peroxidation by iron overloading did not affect and could be more aggra-vated by÷ffsamol supplementation as evidenced by SOD level in liver homogenate.