ABSTRACT
Two experiments were carried out to ascertain if supplementation of a semipurified diet to Swiss-ICR mice with either ascorbic acid (AA), vitamin E (Vit E) or a combination of the two would modulate the carcinogenic effects of N-nitrosopyrrolidine (NPyr) and of its probable precursors (nitrite-N0(2) and pyrrolidine-Pyr) in Experiment I or of NPyr in Experiment II. Results indicated that neither AA nor Vit E modulated the carcinogenic effects of NPyr or of its probable precursors (NO(2) and Pyr). Results verified a previous report from our laboratory showing that NPyr increased the number of malignant tumors by some 5-8 fold over controls. There was a lower incidence of tumors in the control group on the semi-purfied diet than in the groups given NO(2) and Pyr, although both treatments had a low frequency of malignant tumors (1 63 versus 5 72 survivors). Results support our earlier study suggesting that neither NO(2) nor Pyr alone or in combination together contribute to cancer-at least in the laboratory mouse.
ABSTRACT
Odor thresholds for each of the five C(19)-Δ(16)-steroids believed to contribute to boar odor in pork were determined using duo-trio test methodology. Threshold values for 5,16-androstadien-3ß-ol (I) and 4,16-androstadien-3-one (II) were approximately 10 µg/g, whereas those for 5α-androst-16-en-3-one (III), 5α-androst-16-en-3α-ol (IV) and 5α-androst-16-en-3ß-ol (V) were about 1 µg/g. Statistical comparisons of the mean threshold values for each of these compounds showed no difference (P < 0·05) among the mean thresholds of III, IV and V or between compounds I and II. The mean thresholds of compounds I and II were different (P < 0·05) from those of compounds III, IV and V. Triangle test methodology was employed to measure the ability of trained panelists to differentiate the odors of each of these five compounds either singly or in all combinations. Results showed that panelists were able to differentiate (P < 0·05) between the odors of the C(19)-Δ(16)-steroids possessing ketone groups (II and III) and those containing alcohol groups (I, IV and V). Panelists were not able, however, to differentiate (P < 0·05) between the odors of the three alcoholic steroids (I, IV and V), nor were they able to differentiate between the odors of the two ketonic steroids (II and III).
ABSTRACT
Although castration of male pigs grown for meat production has long been a commercial practice in order to eliminate an undesirable odor emanating from the meat upon heating, intact males (boars) grow faster, utilize feed more efficiently and produce leaner carcasses. This review outlines the biochemical pathways of steroid hormone formation in the pig, placing special emphasis on the C19-delta 16-steroids, which have been shown to produce the "urine- or perspiration-like" odor of boar meat. Analytical methods currently available for quantitation of the C19-delta 16-steroids are also reviewed, including gas chromatography-mass spectrometry, radioimmunoassays and enzyme-linked-immuno-absorbent-assays (ELISA). Finally, methods for preventing boar odor are discussed, such as environmental methods of rearing boars, genetic selection against boar odor and autoimmunization against C19-delta 16-steroids. Autoimmunization techniques appear to offer the most promise for inhibiting production of the compounds responsible for boar odor in male pigs raised for meat production, while still maintaining the advantages of improved efficiency and greater leanness.
