Flavor improvement in pork from barrows and gilts via inhibition of intestinal skatole formation with resistant potato starch.

Skatole originates from microbial processing of tryptophan in the large intestine of pigs and accumulates in adipose tissue. Formation may be inhibited by the anti-apoptotic function of butyrate formed out of raw potato starch. Two groups of pigs (each consisting of gilts and barrows) were fed from 30 to 110 kg life weight either a conventional diet (controls; n = 35) or an isocaloric diet containing 300 g of raw potato starch/kg of body weight (RS; n = 34). Skatole concentrations were measured in colon content, blood, and adipose tissue. Odor of cooked meat samples was evaluated by a test panel. RS reduced concentrations in colon content and blood plasma (P < 0.001). Back fat concentrations were decreased significantly from 25 to 1.40 ng/g (barrows; P < 0.001) and from 40 to 9 ng/g (gilts; P < 0.001). Odor rating (scale of 1-5 from very unpleasant to very pleasant) was 3.07 for low skatole concentrations and 2.66 for both medium and high skatole concentrations (P < 0.05).

Estrogen protects against 3-methylindole-induced olfactory loss.

Olfactory dysfunction is among the first signs of Alzheimer's disease (AD). Since estrogen therapy may mitigate the cognitive symptoms of AD, we determined whether 17beta-estradiol (E2) alters the olfactory discrimination performance of female rats exposed to the olfactotoxicant 3-methylindole (3-MI). Twelve ovariectomized rats received daily injections of E2 (1 mg/kg i.p.) in corn oil and 10 received daily injections of corn oil alone. Sensory testing occurred on a near-daily basis throughout a 10-week test period, midway in which a single injection of 3-MI was administered (300 mg/kg i.p.). On each pre- and post-3-MI test day, the rats were required to perform a series of successively more difficult odor discrimination tasks until one was reached where <80% performance was attained. The tasks were between the odor of a 10-4 v/v concentration of ethyl acetate (EA) and the odor of each of six different concentrations of butanol added to the EA (10-4, 10-4.5, 10-5.0, 10-5.5, 10-6.0, 10-6.5 v/v). Following 3-MI treatment, the performance of the E2-treated rats was found to be superior to that of the oil-treated rats and to return more quickly to the pre-3 MI baseline, suggesting that high doses of E2 mitigate 3-MI-induced smell loss in rats. Additional work is needed to determine the physiologic basis of this phenomenon.

Chemical modulation of 3-methylindole toxicosis in mice: effect on bronchiolar and olfactory mucosal injury.

C57BL/6N mice were treated to induce tolerance, to modulate the mixed function oxidase system or to deplete glutathione (GSH) before injection with 400 mg 3-methylindole (3MI)/kg. Effect of pretreatment was determined by histologic comparison of pulmonary and nasal lesions 24 hours after 3MI. beta-Naphthoflavone and 3MI pretreatment significantly decreased 3MI-induced bronchiolar epithelial damage in male and female mice, while phenobarbital protection was significant only in female mice. Only beta-naphthoflavone decreased nasal olfactory epithelial damage. Pretreatment with piperonyl butoxide, SKF 525-A, or alpha-naphthoflavone had no significant effect on development of lesions. Diethylmaleate pretreatment significantly increased mortality and bronchiolar damage in both sexes. Significant differences between male and female mice were not detected in any group. The results suggest that pretreatment with low doses of 3MI or induction of cytochrome P-448 or P-450 protects against 3MI toxicosis while GSH depletion increases mortality and pulmonary lesions.

Effects of 3-methylindole in cattle.

1 Rapid intravenous injection of 3-methylindole (3-MI) was shown to induce an anaphylactoid-like reaction in calves. 2 This was suggested by the reduction in response to a repeat dose of 3-MI, by the reduction of effects in the presence of antagonists to the putative mediators of anaphylaxis in cattle and by the production of signs similar to those seen in experimentally induced bovine anaphylaxis. 3 The plasma half-life of 3-MI was short (14.4 min) and, since absorption of 3-MI from the rumen is known to be slow, the extent of formation of 3-MI from L-tryptophan in the rumen would have to be substantial if 3-MI is to be considered the causative agent of 'fog fever', an acute respiratory distress syndrome seen in cattle.