Gut Microbiota and Its Metabolites in Atherosclerosis Development.

Gut microbiota metabolites have a great influence on host digestive function and body health itself. The effects of intestinal microbes on the host metabolism and nutrients absorption are mainly due to regulatory mechanisms related to serotonin, cytokines, and metabolites. Multiple studies have repeatedly reported that the gut microbiota plays a fundamental role in the absorption of bioactive compounds by converting dietary polyphenols into absorbable bioactive substances. Moreover, some intestinal metabolites derived from natural polyphenol products have more biological activities than their own fundamental biological functions. Bioactive like polyphenolic compounds, prebiotics and probiotics are the best known dietary strategies for regulating the composition of gut microbial populations or metabolic/immunological activities, which are called "three "p" for gut health". Intestinal microbial metabolites have an indirect effect on atherosclerosis, by regulating lipid metabolism and inflammation. It has been found that the diversity of intestinal microbiota negatively correlates with the development of atherosclerosis. The fewer the variation and number of microbial species in the gut, the higher the risk of developing atherosclerosis. Therefore, the atherosclerosis can be prevented and treated from the perspective of improving the number and variability of gut microbiota. In here, we summarize the effects of gut metabolites of natural products on the pathological process of the atherosclerosis, since gut intestinal metabolites not only have an indirect effect on macrophage foaming in the vessel wall, but also have a direct effect on vascular endothelial cells.

Food toxicology: quantitative analysis of the research field literature.

Total-scale quantitative research literature analysis on the food toxicology scientific field has yet to be conducted. In this work, we identified and analysed food toxicology publications in the existing scientific literature. A literature search was performed with the online Web of Science database. Full records and cited references of the 73,099 identified manuscripts were imported into VOSviewer software for analysis. This research field has been growing steadily since the 1990s. Article to review ratio was 7.4:1. The publications were mainly related to toxicology, environmental sciences, food science and technology, pharmacology/pharmacy and biochemistry/molecular biology. The United States and China are major contributors to food toxicology research, followed by other European and Asian countries. The prolific authors have formed three major clusters within a citation network. Toxic or hazardous chemicals related to food with high citations included aflatoxin, dioxin, fumonisin, malondialdehyde, mycotoxin, ochratoxin, phthalate, and polychlorinated biphenyl.

Phytol: A review of biomedical activities.

Phytol (PYT) is a diterpene member of the long-chain unsaturated acyclic alcohols. PYT and some of its derivatives, including phytanic acid (PA), exert a wide range of biological effects. PYT is a valuable essential oil (EO) used as a fragrance and a potential candidate for a broad range of applications in the pharmaceutical and biotechnological industry. There is ample evidence that PA may play a crucial role in the development of pathophysiological states. Focusing on PYT and some of its most relevant derivatives, here we present a systematic review of reported biological activities, along with their underlying mechanism of action. Recent investigations with PYT demonstrated anxiolytic, metabolism-modulating, cytotoxic, antioxidant, autophagy- and apoptosis-inducing, antinociceptive, anti-inflammatory, immune-modulating, and antimicrobial effects. PPARs- and NF-κB-mediated activities are also discussed as mechanisms responsible for some of the bioactivities of PYT. The overall goal of this review is to discuss recent findings pertaining to PYT biological activities and its possible applications.

A comprehensive review on biological properties of citrinin.

Citrinin (CIT) is a mycotoxin which causes contamination in the food and is associated with different toxic effects. A web search on CIT has been conducted covering the timespan since 1946. The accumulated data indicate that CIT is produced by several fungal strains belonging to Penicillium, Aspergillus and Monascus genera, and is usually found together with another nephrotoxic mycotoxin, ochratoxin A. Although, it is evident that CIT exposure can exert toxic effects on the heart, liver, kidney, as well as reproductive system, the mechanism of CIT-induced toxicity remains largely elusive. It is still controversial what are the genotoxic and mutagenic effects of CIT. Until now, its toxic effect has been linked to the CIT-mediated oxidative stress and mitochondrial dysfunction in biological systems. However, the toxicity strongly depends on its concentration, route, frequency and time of exposure, as well as from the used test systems. Besides the toxic effects, CIT is also reported to possess a broad spectrum of bioactivities, including antibacterial, antifungal, and potential anticancer and neuro-protective effects in vitro. This systematic review presents the current state of CIT research with emphasis on its bioactivity profile.

Rapid multiple-level coevolution in experimental populations of yeast killer and nonkiller strains.

Coevolution between different biological entities is considered an important evolutionary mechanism at all levels of biological organization. Here, we provide evidence for coevolution of a yeast killer strain (K) carrying cytoplasmic dsRNA viruses coding for anti-competitor toxins and an isogenic toxin-sensitive strain (S) during 500 generations of laboratory propagation. Signatures of coevolution developed at two levels. One of them was coadaptation of K and S. Killing ability of K first increased quickly and was followed by the rapid invasion of toxin-resistant mutants derived from S, after which killing ability declined. High killing ability was shown to be advantageous when sensitive cells were present but costly when they were absent. Toxin resistance evolved via a two-step process, presumably involving the fitness-enhancing loss of one chromosome followed by selection of a recessive resistant mutation on the haploid chromosome. The other level of coevolution occurred between cell and killer virus. By swapping the killer viruses between ancestral and evolved strains, we could demonstrate that changes observed in both host and virus were beneficial only when combined, suggesting that they involved reciprocal changes. Together, our results show that the yeast killer system shows a remarkable potential for rapid multiple-level coevolution.

Incidence of symbiotic dsRNA 'killer' viruses in wild and domesticated yeast.

Viruses are found in almost all organisms and physical habitats. One interesting example is the yeast viral 'killer system'. The virus provides the host with a toxin directed against strains that do not carry it, while the yeast cell enables its propagation. Although yeast viruses are believed to be common, they have been actually described only for a limited number of yeast isolates. We surveyed 136 Saccharomyces cerevisiae and S. paradoxus strains of known origin and phylogenetic relatedness. Of these, 14 (c. 10%) were infected by killer viruses of one of the three types: K1, K2 or K28. As many as 34 strains (c. 25%) were not sensitive to at least one type of the killer toxin. In most cases, resistance did not disappear after attempts to cure the host strains from their viruses, suggesting that it was encoded in the host's genome. In terms of phylogeny, killer strains appear to be more related to each other than to nonkiller ones. No such tendency is observed for the phenotype of toxin resistance. Our results suggest that even if the killer toxins are not always present, they do play significant role in yeast ecology and evolution.