Disease relevance of Skatole

• Isolation and characteristics of a skatole-producing Lactobacillus sp. from the bovine rumen [1].
• Fecal skatole and indole and breath methane and hydrogen in patients with large bowel polyps or cancer [2].
• These data suggest that fecal skatole excretion equal to or greater than 100 micrograms/g feces might be useful to discriminate colorectal cancer patients from control subjects [2].
• 3MI and Mel produced DNA adducts but not mutations in Salmonella TA100 with S9 [3].
• Control subjects excreting breath methane excreted less fecal skatole than breath methane excretors in the following groups: patients with adenomatous polyps, all patients with colorectal cancer, patients with proximal colon cancer, patients with descending and sigmoid colon cancer, and patients with rectal cancer [2].

High impact information on Skatole

• However, indole, skatole, and toluene increased the affinity of tryptophanase for certain inhibitory amino acids [4].
• Several indole derivatives such as indoline, skatole, oxindole, and 3-methyloxindole are poor competitive inhibitors of MNL with dissociation constants 20-40-fold greater than that for MOI, suggesting a highly specific binding site for the IAA photooxidation product [5].
• Previously, the rate of radical cation decarboxylation to skatole radicals and (skatole) peroxyl radicals was reported to be faster at an acid pH with IAA being more effective than the derivatives [6].
• This suggests that IAA skatole and/or (skatole) peroxyl radicals catalyze lipid peroxidation at pH 6 [6].
• Functional polymorphism in porcine CYP2E1 gene: Its association with skatole levels [7].

Chemical compound and disease context of Skatole

• This is the first report of indoleacetic acid decarboxylation to skatole in pure culture and the demonstration of skatole production by a Lactobacillus species [1].
• The relationship between the pulmonary toxicity of 3- methylindole (3MI, skatole) and the mixed-function oxidase (MFO) system was investigated [8].

Biological context of Skatole

• The aim of this study was to measure the expression pattern of CYP2E1 mRNA in various tissues of the pig, to identify genetic polymorphisms, and to evaluate the functional relevance of polymorphic sites with respect to the skatole level in fat [7].
• Effects of butyrate on apoptosis in the pig colon and its consequences for skatole formation and tissue accumulation [9].
• Responses to the oviposition cue skatole (3-methylindole), presented individually and in combination with the plant-derived and synthetic oviposition pheromone, were also studied [10].
• Detection of quantitative trait loci for androstenone, skatole and boar taint in a cross between Large White and Meishan pigs [11].
• After killing barrows at the end of the feeding period, fat tissue for skatole measurement and colon tissue for histological quantification of mitosis and apoptosis were obtained [9].

Anatomical context of Skatole

• A rapid method for the determination of skatole (3-methylindole) and indole in adipose tissue of pigs by reversed-phase high-performance liquid chromatography has been developed [12].
• Skatole was additionally measured in blood plasma that was sampled daily [9].
• Twenty-four Yorkshire boars and six barrows approximately 8 mo of age were used to evaluate the effects of a GnRH agonist (GnRH-A) on circulating concentrations of LH and testosterone (T), concentrations of skatole in fat, and concentrations of 16-androstene steroids in fat and salivary glands [13].
• Cytochrome P450IIE1 (CYP2E1) is induced by skatole and this induction is blocked by androstenone in isolated pig hepatocytes [14].
• Results show an influence of social rank on plasma concentrations of androstenone (P = .0001) and testosterone (P = .0001), the weight of the bulbourethral glands (P = .0001), and plasma skatole (P = .02) [15].

Associations of Skatole with other chemical compounds

• Rapid determination of skatole and indole in pig back fat by normal-phase liquid chromatography [16].
• A rapid method for the determination of skatole (3-methylindole) in faeces by reversed-phase high-performance liquid chromatography is described [17].
• Evidence exists that butyrate inhibits apoptosis of colon crypt cells in vivo so that less tryptophan from cell debris is available for skatole formation by microbes in the pig colon [9].
• Backfat skatole and salivary gland 16-androstene concentrations were measured from samples taken at slaughter [18].
• Pigs were slaughtered on d 30, and samples of backfat and salivary glands were collected for quantification of skatole and 16-androstene steroid concentrations [13].

Gene context of Skatole

• The characterization of the SULT1A1 gene and its variants should have an important impact on the efforts to develop genetic markers to select for low skatole in pigs [19].
• However, in a population of commercial pigs scored for backfat skatole levels, there was evidence of association between a SNP in the CYP2E1 promoter and skatole deposition, although there was no significant association between this SNP and skatole levels in the experimental cross [20].
• The aim of this study was to isolate and characterize CYP2A6 from pig liver, as well as identify genetic polymorphisms in the CYP2A6 gene, and examine the association between these polymorphisms and skatole level [21].
• There was no effect on skatole levels in backfat (0.141 vs. 0.150 microgram/g) [22].
• Levels of skatole were not associated with the levels of sex steroids, T(3) and IGF-1 [23].

Analytical, diagnostic and therapeutic context of Skatole

• Several skatole metabolites were detected by HPLC, including 6-hydroxyskatole (pro-MII), 3-hydroxy-3-methyloxyindole (MIII), and five others not identified in this study [24].
• SOP and skatole combinations showed additive effects in laboratory assays, but were not tested in field bioassays [10].
• Furthermore, fecal excretion of skatole (inulin = 9.07 vs. control = 18.93 mg/kg DMI) was decreased (P < 0.05) by the inulin supplementation compared with the control group [25].
• Multivariate analysis revealed that gonadal hormones and reproductive organ size influenced prevalence of boar taint, accounting for 30% of the variation in skatole levels in fat and for 37% of the variation in androstenone levels in fat [26].

References