Effects of Phenolic Environmental Estrogens on the Sulfotransferase Activity of the Mouse Intestine and a Human Colon Carcinoma Cell Line, Caco-2

In order to explore the possible role of sulfation in the inactivation of environmental estrogens at gastrointestinal sites and their subsequent removal, we investigated the effects of phenolic environmental estrogens on sulfotransferase (ST) activity. The mouse intestine and a human colon carcinoma cell line, Caco-2, were studied. ST enzymes were found to have a high affinity for diethylstilbestrol (DES) and bisphenol A (BPA), whereas phenol ST (PST) activity was strongly inhibited by nonylphenol and genistein in both mice and humans. Kinetic analysis showed that this inhibition was competitive. These observations suggest that nonylphenol and genistein compounds might inhibit PST activity in the human intestine and that they might escape detoxification by sulfation

Acidic phospholipids directly inhibit DNA binding of mammalian DNA topoisomerase I

AbstractInhibition of mammalian DNA topoisomerase I by phospholipids was investigated using purified enzyme. Acidic phospholipids inhibited the DNA relaxation activity of topoisomerase I whereas neutral phospholipid, phosphatidylethanolamine, did not. Accumulation of a protein-DNA cleavable complex, an intermediate which is known to accumulate upon inhibition by a specific inhibitor camptothecin, did not occur. The filter binding assay revealed that the DNA binding activity of the enzyme was inhibited by acidic phospholipids. Moreoever, direct binding of phosphatidylglycerol to topoisomerase I was demonstrated. These results indicated that the inhibitory effect of acidic phospholipids on topoisomerase I was due to the loss of the DNA binding of the enzyme as a result of direct interaction between phospholipids and the enzyme

Meta-Analysis: Effects of Probiotic Supplementation on Lipid Profiles in Normal to Mildly Hypercholesterolemic Individuals

<div><p>Introduction</p><p>Recent experimental and clinical studies have suggested that probiotic supplementation has beneficial effects on serum lipid profiles. However, there are conflicting results on the efficacy of probiotic preparations in reducing serum cholesterol.</p><p>Objective</p><p>To evaluate the effects of probiotics on human serum lipid levels, we conducted a meta-analysis of interventional studies.</p><p>Methods</p><p>Eligible reports were obtained by searches of electronic databases. We included randomized, controlled clinical trials comparing probiotic supplementation with placebo or no treatment (control). Statistical analysis was performed with Review Manager 5.3.3. Subanalyses were also performed.</p><p>Results</p><p>Eleven of 33 randomized clinical trials retrieved were eligible for inclusion in the meta-analysis. No participant had received any cholesterol-lowering agent. Probiotic interventions (including fermented milk products and probiotics) produced changes in total cholesterol (TC) (mean difference –0.17 mmol/L, 95% CI: –0.27 to –0.07 mmol/L) and low-density lipoprotein cholesterol (LDL-C) (mean difference –0.22 mmol/L, 95% CI: –0.30 to –0.13 mmol/L). High-density lipoprotein cholesterol and triglyceride levels did not differ significantly between probiotic and control groups. In subanalysis, long-term (>4-week) probiotic intervention was statistically more effective in decreasing TC and LDL-C than short-term (≤4-week) intervention. The decreases in TC and LDL-C levels with probiotic intervention were greater in mildly hypercholesterolemic than in normocholesterolemic individuals. Both fermented milk product and probiotic preparations decreased TC and LDL-C levels. Gaio and the <i>Lactobacillus acidophilus</i> strain reduced TC and LDL-C levels to a greater extent than other bacterial strains.</p><p>Conclusions</p><p>In conclusion, this meta-analysis showed that probiotic supplementation could be useful in the primary prevention of hypercholesterolemia and may lead to reductions in risk factors for cardiovascular disease.</p></div

Effects of probiotics on changes in serum HDL-C levels.

<p>Values in parentheses indicate intake duration (weeks). a, b, and c in parentheses indicate Gaio, Stra, and StLa vs PP, respectively; d, e, and f in parentheses indicate Gaio, Stra, and StLa vs PY, respectively. PP: placebo pill; PY: placebo yogurt; StLa: <i>Streptococcus thermophilus</i> and <i>Lactobacillus acidophilus</i>; StLr: <i>Streptococcus thermophilus</i> and <i>Lactobacillus rhamnosus</i>.</p

Funnel plots for the results of the 11 articles in the mean difference in the change in the intervention group (I) minus the change in the control group (C) in TC.

<p>Funnel plots for the results of the 11 articles in the mean difference in the change in the intervention group (I) minus the change in the control group (C) in TC.</p

Subanalysis of changes in TC.

<p>C: control; I: intervention, MD: mean difference, TC: total cholesterol, LDL-C: low-density lipoprotein cholesterol</p><p>Subanalysis of changes in TC.</p

Subanalysis of changes in LDL-C.

<p>C: control; I: intervention, MD: mean difference, TC: total cholesterol, LDL-C: low-density lipoprotein cholesterol</p><p>Subanalysis of changes in LDL-C.</p