The identification of a non-dialyzable proteinase inhibitor with the dialyzable from eggplant exocarps (Agricultural Chemistry)

ナスビ外皮より非透析性のプロテアーゼインヒビターを精製した。塩析, 熱処理, DEAE-セファデックスおよびゲル漏過を用いたが, 最初の段階を除いては, 透析は行わず, 脱塩はすべてダイヤファルターを用いた。このようにして精製したインヒビターは, その分子量, トリプシンやキモトリプシンに対する挙動, またアミノ酸組成の点からみて, 透析性およびアセチル化セルロースを透析に用いて精製したインヒビターと全く同じものであった。そしてナスビ外皮には主要なインヒビターとしては一種類しか存在しないことが明らかとなった。しかし分子量6000のインヒビターが, 未精製のとき, 何故, 透析膜中に残存するかは依然として不明である。Non-dialyzable proteinase inhibtor was purified from eggplant exocarp. The salting out, heat-treatment, DEAE-Sephadex and gel chromatographies were used, and the ultrafiltration was used instead of dialysis except first purification step. The molecular weight, inhibition behaviour for proteinases and amino acid composition were the same as those of purified inhibitor by the other methods. These results show that the non-dialyzable and dialyzable inhibitors are identical and only one kind of inhibitor exists in eggplant exocarp as the main inhibitor. However, the reason why the inhibitor of molecular weight of 6000 in crude stage remains in dialyzing tube, is still unclear

The homogeneity of the purified dialysable proteinase inhibitor from eggplant exocarp (Agricultural Chemistry)

ナスビ果皮より単離精製されたトリプシン・インヒビターの均一性をセフアデックスG-50によるゲルロ過やデイスクおよびSDSポリアクリルアミドゲル電気泳動によって, しらべた。このインヒビター標品は完全に均一な蛋白質であることが判明した。またこのインヒビターはゲルロ過, SDSポリアクリルアミドゲル電気泳動および沈降平衡法によって, 分子量約6000であることが明らかになったが, この値は, 植物由来のインヒビターとして最小のものである。The homogeneity of the protein-like dialysable proteinase inhibitor purified from eggplant exocarp was investigated by gel chromatography on Sephadex G-50 and by disc and SDS-polyacrylamide gel electrophoreses. These analyses showed this inhibitor preparation was homogeneous protein. The molecular weight of this inhibitor was estimated to be approximately 6000 by the methods of gel chromatography, SDS-polyacrylamide gel electrophoresis and equilibrium centrifugation

Hypoxia Stress Test Reveals Exaggerated Cardiovascular Effects in Hypertensive Rats After Exposure to the Air Pollutant Acrolein

Exposure to air pollution increases the risk of cardiovascular morbidity and mortality, especially in susceptible populations. Despite increased risk, adverse responses are often delayed and require additional stress tests to reveal latent effects of exposure. The goal of this study was to use an episode of “transient hypoxia” as an extrinsic stressor to uncover latent susceptibility to environmental pollutants in a rodent model of hypertension. We hypothesized that exposure to acrolein, an unsaturated aldehyde and mucosal irritant found in cigarette smoke, diesel exhaust, and power plant emissions, would increase cardiopulmonary sensitivity to hypoxia, particularly in hypertensive rats. Spontaneously hypertensive and Wistar Kyoto (normotensive) rats, implanted with radiotelemeters, were exposed once for 3h to 3 ppm acrolein gas or filtered air in whole-body plethysmograph chambers and challenged with a 10% oxygen atmosphere (10min) 24h later. Acrolein exposure increased heart rate, blood pressure, breathing frequency, and minute volume in hypertensive rats and also increased the heart rate variability parameter LF, suggesting a potential role for increased sympathetic tone. Normotensive rats only had increased blood pressure during acrolein exposure. The hypoxia stress test after acrolein exposure revealed increased diastolic blood pressure only in hypertensive rats and increased minute volume and expiratory time only in normotensive rats. These results suggest that hypertension confers exaggerated sensitivity to air pollution and that the hypoxia stress test is a novel tool to reveal the potential latent effects of air pollution exposure