Sulforaphane is a naturally occurring isothiocyanate in cruciferous vegetables. Sulforaphane inhibits histone deacetylases, leading to the transcriptional activation of genes including tumor suppressor genes. The compound has attracted considerable attention in the chemoprevention of prostate cancer. Here we tested the hypothesis that sulforaphane is not specific for tumor suppressor genes but also activates loci such as long terminal repeats (LTRs), which might impair genome stability. Studies were conducted using chemically pure sulforaphane in primary human IMR-90 fibroblasts and in broccoli sprout feeding studies in healthy adults. Sulforaphane (2.0 μM) caused an increase in LTR transcriptional activity in cultured cells. Consumption of broccoli sprouts (34, 68, or 102g) by human volunteers caused a dose dependent elevation in LTR mRNA in circulating leukocytes, peaking at more than a 10-fold increase. This increase in transcript levels was associated with an increase in histone H3 K9 acetylation marks in LTR 15 in peripheral blood mononuclear cells from subjects consuming sprouts. Collectively, this study suggests that sulforaphane has off-target effects that warrant further investigation when recommending high levels of sulforaphane intake, despite its promising activities in chemoprevention.

High-resolution 1H nuclear magnetic resonance (NMR) analysis was employed to molecularly screen the lipid, lipid oxidation product (LOP), and antioxidant compositions of four natural (unrefined) cod liver oil (CLO) products. Products 1–3 were non-fermented CLOs, whilst Product 4 was isolated from pre-fermented cod livers. Supporting analytical data that were acquired included biogenic amine, flavanone, tannin, phenolic antioxidant, α-tocopherol, and oxygen radical absorbance capacity (ORAC) determinations by recommended HPLC, LC/MS/MS, or spectrophotometric methods. SDS-PAGE, HPLC, and 1H NMR analyses investigated and determined collagenous antioxidants and their molecular mass ranges. 1H NMR analysis of aldehydic LOPs was employed to explore the susceptibilities/resistivities of each CLO product to peroxidation that is induced by thermal stressing episodes (TSEs) at 180°C, or following prolonged (42 day) storage episodes at 4 and 23 °C. Product 4 displayed extremely high ORAC values, which were much greater than those of Products 1–3, and that were predominantly ascribable to significant levels of peroxidation-blocking and/or aldehyde-consuming collagenous polypeptides/peptides and ammoniacal agents therein. Significantly lower levels of toxic aldehydes were generated in the pre-fermented Product 4 during exposure to TSEs, or the above long-term storage episodes. These results confirmed the enhanced peroxidative resistivity of a fermented, antioxidant-fortified natural CLO product over those of non-fermented unrefined products. Product 4: Green Pasture Blue Ice™ Fermented Cod Liver Oil.

A hybrid catalyst composed of phosphotungstic acid coated cerium oxide nanoparticles was demonstrated to catalyze the one-pot conversion of cellobiose, the disaccharide unit of cellulose, to a monosaccharide mixture of glucose and mannose. A high % conversion of cellobiose (up to 99%) was achieved resulting in a yield of mannose up to 15.8%. The yield of mannose from a glucose starting material was 22.8%, exceeding those of previous ceriumbased glucose epimerization catalysts. The components of the hybrid material were revealed to function synergistically via a two-step process. Cellobiose was hypothesized to be first hydrolyzed to glucose, which was subsequently epimerized to mannose by the cerium ions leached from the catalyst. The 13 C NMR spectroscopic study suggested that the epimerization likely occurred by the way of a 1,2-carbon shift reaction mechanism.

Background Pinto beans contain multiple active agents such as polyphenols, flavonoids, and saponins, and have been shown to lower cholesterol, but the mechanisms involved in this effect have not been explored. Objective This study was to investigate the changes in cholesterol metabolism in response to whole pinto beans (wPB) and their hulls (hPB) supplemented into a diet rich in saturated fat and the molecular mechanisms potentially responsible for these effects in hamsters. Methods Forty-four 9-wk-old male Golden Syrian hamsters were randomly assigned to 4 diet groups (n = 11), including a 5% (wt:wt) fat diet [normal-fat diet (NF)], a 15% (wt:wt) fat diet [diet rich in saturated fat (HSF), saturated fatty acids accounted for 70% of total fatty acids], or HSF supplemented with 5% (wt:wt) wPB or 0.5% (wt:wt) hPB for 4 wk. Plasma, liver, intestinal, and fecal samples were collected to evaluate multiple cholesterol markers and gene targets. Results The plasma non-high-density lipoprotein (non-HDL) concentration was significantly reduced in the wPB- and hPB-supplemented groups by 31.9 ± 3.5% and 53.6 ± 3.2%, respectively, compared with the HSF group (P < 0.01), to concentrations comparable with the NF group. The wPB-supplemented hamsters had significantly lower liver cholesterol (45.1%, P < 0.001) and higher fecal cholesterol concentrations (94.8%, P = 0.001) than those fed the HSF. The expressions of hepatic 3-hydroxy-3-methylglutaryl CoA reductase (Hmgcr) and small intestinal acyl-coenzyme A: cholesterol acyltransferase 2 (Acat2) were significantly decreased in animals administered wPB (by 89.1% and 63.8%, respectively) and hPB (by 72.9% and 47.7%, respectively) compared with their HSF-fed counterparts (P < 0.05). The wPB normalized the expression of Acat2 to the level of the NF group. Conclusion Pinto beans remediated high cholesterol induced by HSF in male hamsters by decreasing hepatic cholesterol synthesis and intestinal cholesterol absorption, effects which were partially exerted by the hulls.