Metabolic Fingerprint of Dimethyl Sulfone (DMSO₂) in Microbial–Mammalian Co-metabolism

There is growing awareness that intestinal microbiota alters the energy harvesting capacity of the host and regulates metabolism. It has been postulated that intestinal microbiota are able to degrade unabsorbed dietary components and transform xenobiotic compounds. The resulting microbial metabolites derived from the gastrointestinal tract can potentially enter the circulation system, which, in turn, affects host metabolism. Yet, the metabolic capacity of intestinal microbiota and its interaction with mammalian metabolism remains largely unexplored. Here, we review a metabolic pathway that integrates the microbial catabolism of methionine with mammalian metabolism of methanethiol (MT), dimethyl sulfide (DMS), and dimethyl sulfoxide (DMSO), which together provide evidence that supports the microbial origin of dimethyl sulfone (DMSO₂) in the human metabolome. Understanding the pathway of DMSO₂ co-metabolism expends our knowledge of microbial-derived metabolites and motivates future metabolomics-based studies on ascertaining the metabolic consequences of intestinal microbiota on human health, including detoxification processes and sulfur xenobiotic metabolism

Convenient Size Analysis of Nanoplastics on a Microelectrode

Chemical recycling is a promising approach to reduce plastic pollution. Timely and accurate size analysis of produced nanoplastics is necessary to monitor the process and assess the quality of chemical recycling. In this work, a sandwich-type microelectrode sensor was developed for the size assessment of nanoplastics. β-Mercaptoethylamine was modified on the microelectrode to enhance its surface positive charge density. Polystyrene (PS) nanoplastics were captured on the sensor through electrostatic interactions. Ferrocene was used as an electrochemical beacon and attached to PS via hydrophobic interactions. The results show a nonlinear dependence of the sensor’s current response on the PS particle size. The size resolving ability of the microelectrode is mainly attributed to the small size of the electrode and the resulting attenuation of the electric field strength. For mixed samples with different particle sizes, this method can provide accurate average particle sizes. Through an effective pretreatment process, the method can be applied to PS nanoplastics with different surface properties, ensuring its application in evaluating different chemical recycling methods

DataSheet1_Integrative evidence construction for resveratrol treatment of nonalcoholic fatty liver disease: preclinical and clinical meta-analyses.ZIP

Background: Resveratrol, a polyphenol found in various plants, is known for its diverse bioactivities and has been explored in relation to nonalcoholic fatty liver disease (NAFLD). However, no high-quality evidence exists regarding its efficacy.Objective: a meta-analysis was conducted to evaluate the potential efficacy of resveratrol in treating nonalcoholic fatty liver disease by analyzing both preclinical studies and clinical trials.Method: PubMed, Embase and Web of Science were searched for the included literature with the criteria for screening. Quantitative synthesis and meta-analyses were performed by STATA 16.0.Results: Twenty-seven studies were included, and the results indicated that resveratrol effectively improved liver function, reduced fatty liver indicators, and affected other indices in preclinical studies. The effective dosage ranged from 50 mg/kg-200 mg/kg, administered over a period of 4–8 weeks. While there were inconsistencies between clinical trials and preclinical research, both study types revealed that resveratrol significantly reduced tumor necrosis factor-α levels, further supporting its protective effect against nonalcoholic fatty liver disease. Additionally, resveratrol alleviated nonalcoholic fatty liver disease primarily via AMPK/Sirt1 and anti-inflammatory signaling pathways.Conclusion: Current meta-analysis could not consistently verify the efficacy of resveratrol in treating nonalcoholic fatty liver disease, but demonstrated the liver-protective effects on nonalcoholic fatty liver disease. The large-sample scale and single region RCTs were further needed to investigate the efficacy.</p

Effect of iron supplementation on cognitive development.

<p>(<b>a</b>) T-maze test scores at PD35. Scores between N-veh and R-veh groups were not significantly different (7.08 ± 0.36 successes vs. 6.08 ± 0.40 successes, <i>p</i> = 0.08) and no differences were found in scores between treatment groups. (<b>b</b>) Passive avoidance test at PD40. Data is expressed as time (s) taken to enter the dark chamber on d2 of the test, designated as retention latency. Latency was significantly decreased in N-150 μg pups compared to the Veh controls (107.54 ± 8.73 s vs. 69.14 ± 11.55 s, * <i>p</i> < 0.05, one-way ANOVA). Data are presented as means ± SEM.</p

Effects of iron supplementation on growth, gut microbiota, metabolomics and cognitive development of rat pups

<div><p>Background</p><p>Iron deficiency is common during infancy and therefore iron supplementation is recommended. Recent reports suggest that iron supplementation in already iron replete infants may adversely affect growth, cognitive development, and morbidity.</p><p>Methods</p><p>Normal and growth restricted rat pups were given iron daily (30 or 150 μg/d) from birth to postnatal day (PD) 20, and followed to PD56. At PD20, hematology, tissue iron, and the hepatic metabolome were measured. The plasma metabolome and colonic microbial ecology were assessed at PD20 and PD56. T-maze (PD35) and passive avoidance (PD40) tests were used to evaluate cognitive development.</p><p>Results</p><p>Iron supplementation increased iron status in a dose-dependent manner in both groups, but no significant effect of iron on growth was observed. Passive avoidance was significantly lower only in normal rats given high iron compared with controls. In plasma and liver of normal and growth-restricted rats, excess iron increased 3-hydroxybutyrate and decreased several amino acids, urea and <i>myo</i>-inositol. While a profound difference in gut microbiota of normal and growth-restricted rats was observed, with iron supplementation differences in the abundance of strict anaerobes were observed.</p><p>Conclusion</p><p>Excess iron adversely affects cognitive development, which may be a consequence of altered metabolism and/or shifts in gut microbiota.</p></div

Plasma metabolite concentrations.

<p>Metabolite concentrations (mean ± SEM) in normal (black) and growth-restricted (grey) rats as a function of iron supplementation (Veh, 30 μg, or 150 μg per day). (<b>a</b>) Plasma amino acids. (<b>b</b>) Other plasma metabolites. (<b>c</b>) Metabolites of possible microbial origin. Abbreviations: 2-Hydroxybutyrate (2-HB); 3-Hydroxybutyrate (3-HB); 2-Hydroxyisobutyrate (2-HIB); 3-Hydroxyisobutyrate (3-HIB); 3-Hydroxyisovalerate (3-HIV), Dimethylsulfone (DMSO₂).</p

Principal coordinates analysis (PCoA) of 16s rRNA.

<p>PCoA of unweighted Unifrac distances of 16S rRNA sequences demonstrates clustering along PC1 based on diet (upper half of the figure) (purple represents restricted and orange as normal) for day 20 and 56. Clustering based on iron supplement (lower half of the figure) (0 μg (Control), 30 μg (medium), or 150 μg (high)).</p

Colon microbial taxa at PD20.

<p>Significantly altered colon microbial taxa by diet at PD20. In red are taxa that increase, and blue are taxa that decrease in growth-restricted rats. The significance was determined using two-way ANOVA (iron treatment X diet) based on relative abundance data. The significance cut-off is <i>p</i> < 0.05. Disclaimer: in this small-scale pilot study (n = 4–6), multiple comparisons were not adjusted, and therefore results may contain false discoveries. Future confirmation is needed.</p

Principal component analysis of plasma metabolites at PD20.

<p>Principal component analysis of plasma metabolite variables from rat pups at PD20 from either a normal (orange) or growth restricted (purple) group. PC1 explains 22.3% of the variation, whereas PC2 explains 18.1%. Inset shows PCA of individual groups colored by amount of iron supplemented. 0 μg (red), 30 μg (green), 150 μg (blue) iron.</p

Hemoglobin, hematocrit and tissue iron content in liver and spleen at PD20.

<p>Hemoglobin, hematocrit and tissue iron content in liver and spleen at PD20.</p