{"title":"Contribution of plasmin to sex differences in platelet aggregation in the rat.","authors":"T Kojima, M Inoue, M Morikawa, Y Horiguchi","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Platelet aggregation was induced more strongly in male than in female 5, 12, and 45 week-old rats by both collagen and arachidonic acid. This is in agreement with our previous reports which suggested that the sex differences in platelet aggregation may be a primary characteristic of rat platelets. In plasma, plasmin-like activity was higher in male than in female rats. Plasmin alone induced aggregation, and low concentrations of plasmin synergistically enhanced collagen-induced aggregation in both male and female rats. Platelets potentiated plasmin generation by plasminogen activator at various Ca2+ concentrations in both male and female rats. Platelets from males displayed more efficient plasmin generation in 2 mM extracellular Ca2+ than those from females. If platelets were activated by abnormal causes in plasma, generated plasmin could make a greater contribution to the potentiated effect of platelet aggregation in male than in female rats. This study suggests that plasmin may be a partial cofactor in sex differences in platelet aggregation in the rat.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"82 3","pages":"351-6"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19115083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Changes in the antioxidant capacity of blood plasma are produced after the ingestion of high doses of fish oil.","authors":"A Garrido, M Garate, A Valenzuela","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Blood plasma shows antioxidant capacity (AOC) due to a number of molecules possessing antioxidant activity. Plasma AOC of young and aged rats fed high doses of fish oil and fish oil + dl-alpha tocopherol was assayed. It was observed that only young rats fed fish oil (with or without antioxidant) show a significant increase in their plasma AOC when compared with controls and with the aged ones. It is suggested that increased AOC results from an adaptive response of animals to the potential risk of oxidative stress due to the increase of membrane polyunsaturation after fish oil ingestion.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"82 3","pages":"367-70"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19115085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Developmental effects of petroleum creosote on mice following oral exposure.","authors":"P R Iyer, T R Irvin, J E Martin","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Petroleum creosote, dissolved in dimethyl sulfoxide, was administered by gavage to pregnant ICR mice on days 5-9 of gestation at a single dose (400 mg/kg body weight per day). Animals were euthanized on day 17 of gestation, and live fetuses were weighed and examined for skeletal and visceral malformations. Maternal body weights were significantly lowered in both the group administered creosote and the group administered the solvent alone. The number of live fetuses, dead fetuses, resorptions, and the sex ratio in the live fetuses were similar in all groups. Petroleum creosote as administered in this study was not found to be teratogenic in ICR mice.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"82 3","pages":"371-4"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19115086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M Asanuma, N Ogawa, H Hirata, Y Kondo, S Nishibayashi, M Yamamoto, A Mori
{"title":"Alterations in the binding of the phosphodiesterase inhibitor, rolipram, after transient ischemia in the gerbil brain.","authors":"M Asanuma, N Ogawa, H Hirata, Y Kondo, S Nishibayashi, M Yamamoto, A Mori","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>To determine ischemia-induced changes in phosphodiesterase (PDE), changes in the membranous binding sites of rolipram, a cAMP-selective PDE inhibitor, were examined in the gerbil brain following transient 5 min forebrain ischemia. Coinciding with the delayed neuronal death (DND) in the hippocampal CA1 region, affinities for cerebral rolipram bindings decreased on Day 4, when intrinsic cAMP, substrate for PDE, might increase. The number of rolipram binding sites was significantly reduced in the hippocampus Day 14, despite the lack of change on Day 4. This reduction in rolipram binding was in agreement with the previously reported late onset reduction of muscarinic receptors, progressing more slowly than DND. Slowly progressive mechanisms may be involved in the ischemia-induced reduction of the hippocampal rolipram binding sites which may be PDEs.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"82 3","pages":"279-85"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19114435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
T Nabeshima, Y Maeda, K Yamada, T Nakamura, T Hasegawa
{"title":"The inhibitory effects of salmon calcitonin on intrathecally-injected N-methyl-D-aspartate-induced aversive behavior in mice.","authors":"T Nabeshima, Y Maeda, K Yamada, T Nakamura, T Hasegawa","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The effects of salmon calcitonin (SCT) on intrathecally-injected N-methyl-D-aspartate (NMDA)-induced aversive behavior were investigated to clarify the involvement of the NMDA receptor/ionophore complex on the analgesic effects of SCT. Intracerebroventricular (i.c.v.) injection of SCT significantly inhibited acetic acid-induced writhing. Intrathecal (i.t.) injection of NMDA (0.25-1.0 nmol/mouse) dose-dependently induced aversive behavior such as scratching and tail biting. SCT at the doses of 0.01 and 0.1 IU/mouse (i.c.v.) significantly inhibited the NMDA-induced aversive behavior. This inhibitory effects of SCT on NMDA (i.t.)-induced aversive behavior were neither potentiated nor antagonized by i.c.v. injection of MK-801 and NMDA, respectively. Further, MK-801 (i.c.v.) and NMDA (i.c.v.) themselves did not affect the NMDA (i.t.)-induced aversive behavior. These results suggest that the NMDA receptor/ionophore complex in the brain is not directly involved in the antinociceptive effects of intracerebrally-injected SCT.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"82 2","pages":"175-84"},"PeriodicalIF":0.0,"publicationDate":"1993-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19290662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Protective effect of dantrolene sodium on carbon tetrachloride induced liver injury in the rat.","authors":"F Yamagishi, T Komoda, K Ohnishi, S Itoh","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The effect of dantrolene sodium on liver injury induced by CCl4 was investigated in the rat. Liver microsomal P-450 and b5 levels, serum triiodothyronine levels (T3), and alanine aminotransferase activity (ALT) were measured over 4 to 16 h after CCl4 (0.2 ml/kg, s.c.) administration. Serum ALT rose following CCl4 administration, while liver cytochrome P-450 and b5 levels and serum T3 which reflects the liver microsomal thyroxine-5'-deiodinase activity (1) fell. Intraperitoneal administration of dantrolene sodium (5 mg/kg), 1 h before CCl4 s.c., suppressed CCl4-induced elevation of the serum ALT significantly. However, levels of P-450, b5, and serum T3 were not significantly different between dantrolene-treated and untreated groups. These results suggest that dantrolene sodium has a protective effect on CCl4-induced liver injury through a mechanism unrelated to these liver microsomal functions.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"82 2","pages":"237-40"},"PeriodicalIF":0.0,"publicationDate":"1993-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19289694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
P Ballerini, R Ciccarelli, P Di Iorio, P Giuliani, D Francano, G Fanò, F Caciagli
{"title":"TMB-8 and thapsigargin modulate purine release from dissociated primary cultures of rat brain astrocytes.","authors":"P Ballerini, R Ciccarelli, P Di Iorio, P Giuliani, D Francano, G Fanò, F Caciagli","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In our previous studies, the evoked purine outflow from rat brain cultured astrocytes was reported to be Na+ independent and K+ and [Ca2+]e partially dependent. Thus, the eventual [Ca2+]i influence on purine astrocyte release was investigated in an attempt to better characterize the ionic requirements of this mechanism in cells which serve many complex and still partly unknown functions within the CNS. TMB-8 and Thapsigargin (drugs described as able to inhibit and increase the ion efflux from its internal stores respectively) and BAPTA/AM (able to chelate the cytoplasmic free Ca2+), were used. TMB-8 and BAPTA/AM decreased, whereas Thapsigargin enhanced glial purine outflow. These findings suggest a significant [Ca2+]i dependence of the electrically evoked purine efflux from cultured astrocytes even though further investigations using fluorescent probes are needed.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"82 2","pages":"167-74"},"PeriodicalIF":0.0,"publicationDate":"1993-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19290661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
C B Nyathi, N Dube, J A Hasler, M J Obwolo, H Fuhrmann, H P Sallmann
{"title":"The effect of diet on aflatoxin B1 binding to hepatic macromolecules in rats.","authors":"C B Nyathi, N Dube, J A Hasler, M J Obwolo, H Fuhrmann, H P Sallmann","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Fischer 344 rats were fed a low-fat high carbohydrate diet (HC), an isocaloric fat-containing diet (IC), a hypercaloric fat-containing diet (HF) or rat chow. Covalent binding of AFB1 to liver DNA, RNA and total proteins was investigated in a 24 hour period following administration of a single intraperitoneal dose of AFB1 (1 mg/kg body weight). AFB1 binding to nucleic acids was greatest in the HC and was generally significantly lower (p < 0.05) in the HF, IC and rats fed chow. The results suggest that fat decreases hepatic macromolecular adduct formation by inhibiting activation of AFB1 to the epoxide or by enhancing the activity of detoxification pathways.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"82 2","pages":"199-207"},"PeriodicalIF":0.0,"publicationDate":"1993-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18516657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Immunoreactive hepatocyte growth factor is present in tissue extracts from human breast cancer but not in conditioned medium of human breast cancer cell lines.","authors":"J Yamashita, M Ogawa, T Beppu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Hepatocyte growth factor (HGF) is a novel mitogen for mature hepatocytes. In the present study, we have measured immunoreactive (ir)-HGF concentration in tumor extracts of 82 primary human breast cancers using an enzyme-linked immunosorbent assay (ELISA). Ir-HGF was detectable in all tissue extracts, the concentration ranging from 1.4 to 306.5 ng/100 mg protein (median value: 11.2 ng/100 mg protein). Correlation analyses between ir-HGF concentration and clinicopathological factors showed that the ir-HGF level was significantly higher in tumors with sizes of more than 5.0 cm compared with those less than 5.0 cm. In contrast, no detectable amount of ir-HGF was secreted into culture medium of two breast cancer cell lines, MCF-7 and ZR-75-1, suggesting that the cancer cell itself has no ability to produce ir-HGF.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"82 2","pages":"249-52"},"PeriodicalIF":0.0,"publicationDate":"1993-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19289697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Antioxidant and pro-oxidant assay for a new drug GEPC: detected by ESR spectrometry and by protective effects on lipid peroxidation and biomolecule degradation.","authors":"J Liu, A Mori, K Ogata","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>L-Ascorbic acid 2-(20 beta-11-oxo-olean-12-en-29-oic acid ethylester-3-beta-yl hydrogen phosphate) sodium salt (GEPC) is a newly synthesized compound representing a phosphate diester linkage of glycyrrhetic acid ethylester and ascorbic acid. In the present study, we found that GEPC effectively inhibited Fe(III)-ADP/NADPH-induced peroxidation of liver microsomes. The inhibitory effect was much greater than that of glycyrrhetic acid (GA), and contrasted with the stimulatory effect of ascorbic acid. An ESR study showed that GEPC appeared to have a great loss of the DPPH and superoxide radical scavenging effects of ascorbic acid. However, GEPC, like ascorbic acid, inhibited hydroxyl radicals generation in both Fe(II)-H2 O2 and Cr(VI)-H2 O2 systems. GEPC, unlike ascorbic acid, showed no pro-oxidant effect and acted as an effective iron-chelating agent in the ESR study or in the iron-induced deoxyribose and DNA degradation assays. The hydroxyl radical scavenging effect of GEPC was further demonstrated by its protective effect on the hydroxyl radical- induced degradation of certain biomolecules, i.e., carbohydrates, amino acids, and DNA. These results demonstrate that beside its protective effect on ascorbic acid autoxidation and increasing water solubility of GA, GEPC is also an antioxidant though not so powerful as ascorbic acid but more powerful than GA.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"82 2","pages":"151-66"},"PeriodicalIF":0.0,"publicationDate":"1993-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19290660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}