Use of Lilium longiflorum, cv. ace pollen germination and tube elongation as a bioassay for the hepatocarcinogens, aflatoxins.

Although various animal tissues are used for bioassay of aflatoxins (B1, B2, G1, G2), a rapid bioassay dependent upon a plant part's response does not exist. Both pollen germination (G) and tube elongation (TE) were enhanced in a 3.0 mM KH2PO4 (K)-containing but AFB1-lacking, modified Dickinson's medium. The B1 did not affect G when K was withheld but K supplementation impaired G above 15 micrograms/ml B1. Without K, 5-20 stimulated but 25 and 30 micrograms/ml B1 inhibited TE which was suppressed by every B1 conc tested in K-containing medium. Addition of NaH2PO4(N) instead of K to medium did not promote G. Slight G stimulation occurred at 16.6 micrograms/ml mixed aflatoxins (MA) in medium lacking either K or N but low G inhibitions were observed with K or N. The MA at 33.3 micrograms/ml reduced G 2.5% in K's of N's absence and 26 or 17% in their presence. While K did not stimulate TE without MA, N did 26%. At 16.6 and 33.3 micrograms/ml MA, TE was reduced 19, 6, 19% and 24, 25, 31%, respectively, in control, K- and N- media. Pollen G and TE were markedly sensitive to G1. Significant inhibitions of Zea mays seed G were observed at 5.8 and 11.6 micrograms/ml B1 but not root elongation (RE) from 0.4-11.6 micrograms/ml. The MA (31.5 micrograms/ml) administered for 72-240 hr did not influence either Arachis hypogeae seed G or RE. However, imbibing 5 cultivars each of Avena sativa (65-117 hr) and Hordeum vulgare (39-89 hr) inhibited RE 4/15-62%. Thus, except for Z. mays, pollen G and TE appear to be more B1-sensitive than seed G and RE. But, the pollen bioassay is less sensitive than both certain animal bioassays (0.025 micrograms/ml) and analytical methodologies (10 pg.).

Influence of estradiol on accessory reproductive organs in the castrated male rat. Effects of bromocriptine and flutamide.

Estradiol partially maintained the weights of the dorsolateral prostate and seminal vesicles in castrated adult male rats. One group of animals received subcutaneous injections of estradiol (0.01 mg/kg) daily, while a second group of animals received estradiol plus bromocriptine (4.0 mg/kg). Changes in weights of accessory reproductive organs were correlated with serum prolactin levels. Estradiol significantly increased serum prolactin levels while concomitant treatment with bromocriptine caused serum prolactin to remain at castrate levels. Bromocriptine slightly decreased, but did not abolish, the effect of estradiol on weights of the dorsolateral prostate and seminal vesicles. To determine if the effect of estradiol was mediated by androgen receptors in the dorsolateral prostate and seminal vesicles, a third group of animals was treated with flutamide. Flutamide, at a dosage (20 mg/kg) that abolished the effects of dihydrotestosterone on the weights of these tissues, produced no alternation of the effects of estradiol. Treatment of animals with a combination of flutamide, bromocriptine, and estradiol did not significantly alter organ weights from the results obtained with bromocriptine and estradiol. Scatchard plot analysis of the effect of estradiol treatment on cytosol binding of estradiol demonstrated increased quantities of estradiol binding in dorsolateral prostate and seminal vesicles which correlated with the changes in weights noted. Although part of the effect of estradiol on regression of male accessory reproductive organs of castrated rats may be mediated by prolactin, the principal effect appears to be a direct action on responsive tissues.