Histamine release on rat pleural and peritoneal mast cells elicited by human GRF(1-29)NH2.

We have studied the release of histamine elicited by human GRF(1-29)NH2 on rat peritoneal and pleural mast cells. The secretion is temperature dependent, the release being optimal at 37 degrees C, and it can be inhibited with antimycin A. The activation of pleural and peritoneal mast cells is similar, but there is a slight inhibition for both populations after purification with Percoll.

Effect of purification, theophylline and sodium fluoride on histamine release produced by antineoplastic drugs on rat mast cells. A distinctive mechanism of action for carboplatin.

The antineoplastic drugs, cytarabine, ifosfamide, vinorelbine, doxorubicin, asparaginase and carboplatin, elicit histamine release from rat pleural and peritoneal mast cells. Both cell populations do not show heterogeneity in their response to stimulation by any of these drugs, with the exception of cytarabine, which activates pleural mast cells at lower concentrations. When these cells are purified with Percoll, L-asparaginase, vinorelbine and cytarabine completely lose their capability of inducing histamine release in both cell populations, while the other drugs still show the same pattern of response as with unpurified cells. These results indicate that some membrane component crucial for the action of vinorelbine, L-asparaginase and cytarabine is lost during the purification procedure. Pretreatment of the cells with theophylline completely inhibits the response to cytarabine, ifosfamide, vinorelbine and asparaginase, and inhibits the response to doxorubicin by up to 75% only. Theophylline does not change the response to carboplatin. Sodium fluoride does not change the response to any of the drugs tested, with the exception of carboplatin, in which case a complete inhibition is observed. In conclusion, carboplatin activates rat mast cells through a completely different mechanism of action with respect to the other drugs studied.

Non-immunological release of histamine from rat mast cells elicited by antineoplastic agents.

We studied the histamine-releasing activity of several antineoplastic drugs on rat pleural and peritoneal mast cells. The drugs tested included the nitrogen mustards cyclophosphamide and ifosfamide, the nitrosourea carmustine, the triazene dacarbazine, the folic acid analogue methotrexate, the pyrimidine analogue cytarabine and fluorouracil, the vinca alkaloids vinblastine, vincristine and Vinorelbine, the epipodophyllotoxins etoposide and teniposide, and the enzyme L-asparaginase. Methotrexate, carmustine, fluorouracil, vinblastine and vincristine failed to elicit histamine release on rat mast cells. All of the other drugs evoked histamine release in both the presence and the absence of extracellular calcium, but ifosfamide, cytarabine and asparaginase induced a much lower release in the absence of this cation. The response elicited by cytarabine and etoposide was much higher in pleural than in peritoneal mast cells. These results indicate that some antineoplastic drugs may directly activate the release of histamine, which could contribute to some of their secondary effects.

Nonimmunological release of histamine from rat mast cells elicited by antineoplastic agents: effect of drug combinations.

We studied the release of histamine elicited by some antineoplastic drugs in rat pleural and peritoneal mast cells. The drugs tested included the antibiotic mitomycin; the anthracyclines daunorubicin, doxorubicin, and epirubicin; the glycopeptide bleomycin; the chromopeptide dactinomycin; the platinum coordination complexes carboplatin and cisplatin; and the anthracenedione mitoxantrone. Mitomycin and bleomycin failed to elicit any release of histamine, whereas all of the other drugs induced histamine release from either pleural or peritoneal mast cells, the release being independent of extracellular calcium. The results indicate that antineoplastic drugs activate histamine release in a manner similar to that shown by compound 48/80, which may contribute to some of their secondary effects.

Variations in monoamine contents in discrete brain regions and their concomitance with plasma corticosteroids during the day.

We determined the plasmatic corticosterone and 5-HT, NA and DA levels in the hypothalamus, amygdala, hippocampus and septum at different hours. Significant fluctuations were found to occur in the biogenic amines and corticosterone plasmatic levels. Highest levels of this hormone were detected at the end of the light period. Plasma corticosterone was found to be inversely correlated with 5-HT and DA levels of amygdala and directly correlated with hypothalamus DA level.