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PubMed1987

Antipain microinjection prevents progesterone to inhibit adenyl cyclase in Xenopus oocytes.

Microinjection of antipain, an inhibitor of thiol and Ca2+-dependent proteases, in immature Xenopus oocytes inhibited meiotic maturation induced by progesterone, but not by transfer of cytoplasm taken from maturing oocytes. Oocytes could be released from antipain inhibition by increasing progesterone concentration. alpha-32P-ATP was microinjected to study adenylcyclase in ovo. As already reported, neosynthesis of cAMP was decreased following progesterone application. This decrease was not observed, or it was considerably reduced, in oocytes previously injected with antipain. In amphibian, full-grown ovarian oocytes are arrested at first meiotic prophase, and have a large nucleus known as the germinal vesicle. Progesterone induces the production of a cytoplasmic maturation-promoting factor (MPF), which itself triggers germinal vesicle breakdown (GVBD), and subsequent events of meiotic maturation (Masui and Markert, 1971; Gerhart et al., 1984). A considerable body of evidences support the view that release from prophase block is due to inactivation of a cAMP-dependent protein kinase (reviewed by Maller, 1983). On the other hand, progesterone has been shown to induce a transient decrease in cAMP level (Speaker and Butcher, 1977; Schorderet-Slatkine et al., 1982; Cicirelli et al., 1985), and this initial drop of cAMP, along with a number of studies indicating a decrease in adenylate cyclase activity (Mulner et al., 1979; Baltus et al., 1981; Sadler and Maller, 1981; Finidori-Lepicard et al., 1981; Jordana et al., 1981), provided key support to the theory that an early drop in cAMP led to the dephosphorylation of a hypothetical protein which initiates maturation.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed1984

Inhibition of Leishmania amastigote growth by antipain and leupeptin.

Antipain and leupeptin were found to be potent inhibitors of the growth of Leishmania mexicana mexicana amastigotes in explanted mouse unstimulated peritoneal macrophages. Antipain at 100 mg l-1 reduced eight-fold the percentage of macrophages infected and to 5% of the control the number of amastigotes present after seven days incubation. At 1 mg l-1, antipain and leupeptin were as effective antileishmanial agents as pentamidine isethionate, all three stopping parasite multiplication over the seven-day incubation.

Animals↗
PubMed1985

Inhibition of fibrinogen receptor expression and serotonin release by leupeptin and antipain.

Human platelet agonists such as thrombin, ADP, and collagen stimulate the rapid expression of fibrinogen receptors. In other cell types, calcium-activated proteases have been suggested to participate in the mechanism of expression of cell surface receptors (Lynch, G., and Baudry, M. (1984) Science 224, 1057-1063). In platelets the majority of the neutral protease activity is calcium-activated protease. We examined the effects of leupeptin and antipain, two calcium-activated protease inhibitors, on the expression of platelet fibrinogen receptors. These inhibitors abolished thrombin and ADP-induced fibrinogen binding. This inhibition required the addition of leupeptin or antipain prior to the agonist and was not due to displacement of fibrinogen from its receptor or inhibition of agonist binding to platelets. Leupeptin and antipain also inhibited fibrinogen-independent thrombin-stimulated release of serotonin. These results are discussed in relation to the involvement of calcium-activated protease in early events of platelet activation.

Antipain↗
PubMed1983

Antiteratogenic effects of tumor inhibitors, caffeine, antipain, and retinoic acid in mice.

To learn the effects of tumor inhibitors on chemically induced malformations, caffeine, antipain, and 13-trans-retinoic acid were given to pregnant ICR/Jcl mice after a single dose of urethan, N-hydroxyurethan, N-methyl-N-nitrosourea, N-ethyl-N-nitrosourea, or 4-nitroquinoline 1-oxide, which induces about 50% of the malformed fetuses. When caffeine was given immediately after carcinogen treatment on Day 10, urethan- and N-ethyl-N-nitrosourea-induced malformations were significantly suppressed by caffeine posttreatment, while N-hydroxyurethan- and N-methyl-N-nitrosourea-induced malformations were not suppressed by caffeine. 4-Nitroquinoline 1-oxide-initiated teratogenesis was also suppressed, but not significantly so (p not equal to 0.07). The results were very similar to those of the effects of caffeine on tumors induced by these carcinogens. Malformations of genetic origin (cleft palates and cleft lips) in CL/Fr mice were also suppressed significantly by caffeine treatment on Days 8 to 11, although the level of inhibition was less than that in chemically induced malformations. A protease inhibitor (antipromotor), antipain, also suppressed urethan-induced malformations. The antiteratogenic effects of antipain were most effective when it was given during the period of 24 to 48 hr after urethan treatment, while those of caffeine were most effective when it was given immediately after urethan. The promoting process might be involved in chemically induced teratogenesis, as it was in carcinogenesis. A natural retinoid (13-trans-retinoic acid) also suppressed urethan-induced malformations. Thus, tumors and malformations induced by chemical carcinogens were suppressed by tumor inhibitors, suggesting the similarity of both processes in the subcellular level, in spite of their morphological differences.

4-Nitroquinoline-1-oxide↗
PubMed1977

Antipain and leupeptin restrict uterine DNA synthesis and function in mice.

As in rats, administration of estradiol to ovariectomized mice results in a trypsin-like proteolytic activity in the uterus. After fractionation of uteri from estradiol-treated ovariectomized mice the protease activity was found in the 12,000 times g pellet and the nucleus, appearing first in the former. Further fractionation of the pellet by discontinuous sucrose gradient centrigugation resulted in sedimentation of the protease with 5'-nucleotidase, a marker enzyme for plasma membrane and separate from mitochondrial and lysosomal enzyme markers. Solubilization was best accomplished by lysis at 37 degrees. The soluble enzyme from mouse uterus had optimal activity at about 43 degrees and pH 8.3 and was inhibited by diisopropylfluorophosphate, tosylarginine methyl ester, antipain, and leupeptin, but not by soybean trypsin inhibitor. Inhibition in vitro by antipain and leupeptin, two low molecular weight peptides, prompted the study of their effect in vivo on the mouse uterus. After intact, cycling female mice received subcutaneous injections of antipain and leupeptin for 16 days, their uteri showed significant diminution in weight and total DNA when compared to untreated controls. Fertility rates were also diminished. Trypsin-like protease activity may be essential to normal uterine metabolism and function.

Animals↗
PubMed1979

Antipain lethality to Escherichia coli: dependence upon cyclic adenosine 3',5'-monophosphate and its receptor protein.

Antipain kills Escherichia coli K-12 cells in an exponential manner beginning 1 h after its addition. Mutant strains, delta cya and crp, which are unable to synthesize cyclic adenosine 3',5'-monophosphate (cAMP) and the cAMP receptor protein, respectively, are not affected. Addition of cAMP (5 mM) to antipain-treated mutant strains causes killing of delta cya cells, but not crp cells. Thus the lethal effect of antipain is dependent upon cAMP and its receptor protein.

Cyclic AMP↗
PubMed1982

Antipain, but not cycloheximide, suppresses radiation transformation when present for only one day at five days post-irradiation.

It has previously been observed that protease inhibitors suppress radiation transformation in vitro. In the experiments reported here, it was observed that a 24 h treatment with the protease inhibitor antipain at five days post-irradiation was sufficient to significantly suppress radiation transformation. Comparable experiments performed with cycloheximide, an inhibitor of protein synthesis, showed that this metabolic inhibitor could suppress radiation transformation when present immediately following the X-ray exposure but not when present for one day at five days post-irradiation. These results suggest that antipain is suppressing an ongoing cellular process occurring in response to X-irradiation.

Animals↗
PubMed1987

Reversible conversion of tyrosine hydroxylase to an inactive form by antipain.

Tyrosine hydroxylase, the rate-limiting enzyme in the biosynthesis of catecholamines, was reversibly inactivated by incubation with antipain, which is known as a microbial protease inhibitor. The inactivation was a time-dependent reaction and it was prominent when the enzyme was assayed at a neutral pH but not when assayed at an acidic pH. The inactivated enzyme was markedly activated by cyclic AMP-dependent protein kinase. Other microbial protease inhibitors such as leupeptin, chymostatin, and pepstatin did not induce such as inactivation of the enzyme.

Animals↗
PubMed1980

Antipain and 12-O-tetradecanoyl-phorbol-13-acetate: phenomenology of effects on UV mutagenesis in V79 Chinese hamster cells.

Antipain (AP) and 12-O-tetradecanoyl-phorbol-13-acetate (TPA) were tested in V79 Chinese hamster cells for cytotoxicity and effects on survival and 6-thioguanine-resistant (6-TGr) mutation after UV-irradiation. AP and/or TPA were relatively non-cytotoxic and had no significant effects on UV survival. Despite their non-mutagenicity, the recovery of UV-induced 6TGr colonies was significantly enhanced by the pretreatment with either AP (0.5-2 mM) or TPA (0.1-1 microgram/ml) only during the expression period before the 6TG selection at a low density of cells in the absence of AP or TPA. Such enhancing effects were maximal when AP or TPA was present during the late expression period after the mutation fixation and extensive dilution of DNA lesions. Reconstruction experiments revealed the antagonistic actions that TPA and AP tended to eliminate and increase, respectively, the metabolic co-operation. In the TPA-plus-AP treatment, AP abolished the TPA-enhanced recovery of induced mutants. Thus, it seems that TPA increases the mutant recovery largely through decreased metabolic co-operation and AP could modulate the mutation expression. Further, an error-prone inducible repair may not exist, or, if it exists, AP may not inhibit it in V79 Chinese hamster cells.

Animals↗
PubMed1989

c-fos mRNA levels are reduced in the presence of antipain and Bowman-Birk inhibitor.

We have studied whether the Bowman-Birk protease inhibitor (BBI) could affect the expression of c-fos in BALB/c/3T3 cells stimulated to divide with serum. Our results show that the levels of c-fos message are significantly decreased in the presence of antipain and BBI. When the cells were treated with cycloheximide after being grown in the presence of BBI, there was no significant decrease in mRNA levels. Our experiments suggest that a BBI-inhibitable protease may be necessary for c-fos expression in 3T3 cells and that new protein synthesis is required for this hypothesized protease to be active. As BBI is capable of affecting c-fos gene expression in cells without being present in the nucleus, our results suggest that a novel pathway could be involved in c-fos gene expression.

Animals↗
PubMed1981

Antipain and radiation effects on oncogenic transformation and sister chromatid exchanges in Syrian hamster embryo and mouse C3H/10T1/2 cells.

Depending on its time of addition to Syrian hamster embryo or mouse C3H 10T1/2 cells the protease inhibitor antipain (AP) can enhance, or reduce, radiation induced-oncogenic transformations. These opposing influences are not paralleled by changes in sister chromatid exchanges in either cell system. A 24 h treatment with 10 microM AP prior to, and during irradiation, with removal 10 min after irradiation results in greater than a two-fold increase in transformants. Conversely, a 24 h treatment beginning 10 min after irradiation results in about a two-fold decrease in transformants. The utility of AP as an agent for the reduction of tumorigenesis is brought into question, since quite short temporal differences in application can result in near five-fold differences in the frequencies of oncogenic transformations.

Animals↗
PubMed1984

Protease inhibitor antipain reduces nuclear binding of estrogen-receptor complex in MCF-7 breast tumor cells.

We have initiated studies to ascertain the effects of protease inhibitors on specific steroid hormonal-related events as they occur in cultured cells, in an attempt to identify hormone-related processes perturbed by these inhibitors. We report here that the presence of antipain during incubation of cultured MCF-7 breast tumor cells with estradiol-containing medium considerably reduces the extent of nuclear binding of the estradiol-receptor complex.

Antipain↗
PubMedDate not supplied

Effects of the protease inhibitor antipain on cell malignant transformation.

BACKGROUND: Several natural products have been found to exhibit a chemopreventive activity both in in vivo and in vitro experimental systems. Among them, protease inhibitors seem to play a key role in the regulation of growth and phenotypic expression of transformed cells as well as in the regulation of the late events of carcinogenesis. We evaluated the effect of antipain (AP), a natural protease inhibitor, on chemically induced BALB/c 3T3 cell transformation, on invasion and chemotactic motility of transformed cells and on their gelatinase expression. METHODS: BALB/c 3T3 cells were plated and exposed to 2.5 micrograms/ml 3-MCA or 50 micrograms/ml, 1,2-DBE. The effect of a non-cytotoxic dosage of AP (10 microM) was studied by: a) pretreating cells with AP for 48 hours before the carcinogen exposure; b) adding AP simultaneously to the carcinogen treatment; c) chronic addition of AP at each medium change throughout the experimental duration. The effectiveness of the treatment was analysed as the ability to reduce or inhibit the occurrence of transformed foci. Modulation of the invasive phenotype by anti-transforming dosages of AP was evaluated by in vitro Matrigel invasion assay. Gelatin zymography was performed in order to assess AP regulation of proteolytic enzymes, such as metalloproteases, involved in invasion and metastasis. RESULTS: AP treatment can reduce the transformation rate both in 3-MCA- and 1,2-DBE-initiated cells. Its effectiveness depends on the administration schedule, and chronic addition seems to be the most effective treatment. The concentration of AP, which is effective in the antitransformation assay, is not able to significantly affect the migration and invasion of chemically transformed cells or their gelatinase activity. CONCLUSIONS: AP can suppress chemically induced BALB/c 3T3 cell transformation through mechanisms which do not involve modulation of the invasive phenotype.

3T3 Cells↗
PubMed1991

Antipain-induced suppression of oncogene expression in H-ras-transformed NIH3T3 cells.

Antipain (AP; 50 micrograms/ml) inhibits transformation of NIH3T3 cells after transfection with an activated H-ras oncogene. To determine whether AP effects on transformation are associated with alterations in oncogene expression, NIH3T3 cells were cotransfected with an activated H-ras oncogene and the selectable marker gene aph, and gene expression was quantified. Fifty percent of geneticin-resistant colonies which were exposed to AP failed to express the transformed phenotype as determined by their inability to grow in soft agar. Northern blot analysis of the transformed and nontransformed colonies revealed that suppression of H-ras transformation by AP was associated with a decrease in expression of the exogenously transfected H-ras gene by approximately 4-fold. Expression of the endogenous oncogene c-myc was decreased by approximately 2.5-fold, to levels seen in untransfected cells. AP-treated colonies that retained the transformed phenotype had levels of oncogene expression that were similar to untreated ras-transformed colonies. Southern blot analysis revealed no effects of AP on incorporation or copy number of the H-ras gene.

Animals↗
PubMed1990

[Transcription of nucleoplasmatic and nucleolar sites of DNA sensitive to the protease inhibitor antipain].

Age-related changes in the transcriptional activities of Purkinje cells chromatin and sympathetic cranial cervical ganglion under the influence of morphine and some natural and synthetic peptide compounds were found. It was shown that at different stages of the ontogenesis, morphine was capable of increasing the template activity of nucleolar and/or extranucleolar chromatin, and that this process was inhibited by antipain. The findings suggest the presence of DNA sites in the eucaryotic genome, that are induced by the protease mechanism and are likely to be similar to the SOS-genes of procaryotes. The SOS-genes of procaryotes are activated under unfavourable conditions and promote the survival of the microbial population, while in eucaryotes these genes are believed to provide the formation of definite cell populations whose composition is the most adequate for the living conditions of an adult organism.

Animals↗
PubMed1977

[Inhibition of the reinitiation of meiosis in Xenopus laevis oocytes by three natural antiproteases: antipain, chymostatin, and leupeptin].

Oocytes incubated for 1 hr. in saline containing 1 mg/ml of antipain, leupeptin or chymostatin do not reinstate meiosis when progesterone or ionophore A 23187 are added. On the contrary such oocytes remain able to undergo meiosis when injected with cytoplasm of maturing oocytes (MPF), with Rabbit phosphorylase kinase or with Beef protein kinase. These results demonstrate that the loss of responsiveness to progesterone or ionophore is not due to toxic effects but rather to some interference with a key event which occurs prior to MPF action.

Animals↗