Meat crust as a novel food ingredient to regulate lipid peroxidation and oxidative stress.

Pan Fry (PF) is a common heating treatment however, there is limited data on meat oxidation after PF using direct contact with an uncoated iron pan. After PF, a crust is formed, and in this study, we aim to evaluate the potential anti-oxidation and anti-lipid peroxidation capacity of such crust. Ground beef and turkey meat were heat treated using PF or microwave. Lipid peroxidation was evaluated using malondialdehyde accumulation. PF meat generated lower lipid peroxidation levels versus microwave-heated meat. Iron PF has decreased lipid peroxidation versus Teflon pan heating. The crust significantly lowered lipid peroxidation and possessed millard reaction products (MRPs), strong reducing abilities, iodine removal capacity, and some iron chelation capacity. We demonstrated that the crust substantially decreases lipid peroxidation levels in various systems and can be used as a novel seminatural antioxidant ingredient, which may lead to extended shelf life and protects various food products.

DMF-Activated Nrf2 Ameliorates Palmitic Acid Toxicity While Potentiates Ferroptosis Mediated Cell Death: Protective Role of the NO-Donor S-Nitroso-N-Acetylcysteine.

Nonalcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease that can develop into an aggressive form called nonalcoholic steatohepatitis (NASH), which ultimately progresses to cirrhosis, hepatocellular carcinoma (HCC), and end-stage liver failure. Currently, the deterioration of NAFLD is attributed to specific lipid toxicity which could be due to lipotoxicity and/or ferroptosis. In the current study, we evaluated the involvement of the nuclear factor erythroid 2 (NFE2)-related factor 2 (Nrf-2), which is a main activator of phase II metabolism in the two types of lipid-induced toxicity in hepatocytes, lipotoxicity by saturated fatty acids, and in ferroptosis, and the effect of NO donor treatment. AML12 cells were exposed to 600 µM palmitic acid to induce lipotoxicity or treated with 20 µM erastin or 5 µM RSL3 for ferroptosis. In SFA-lipotoxicity, pretreatment with the Nrf2 activator dimethyl fumarate (DMF) managed to ameliorate the cells and the oxidative stress level while aggravating ferroptosis due to emptying the thiol pool. On the other hand, the nitric oxide (NO)-donor, S-nitroso-N-acetylcysteine (NAC-SNO) proved to be effective in the prevention of hepatocytes ferroptosis.

Antimicrobial and Antiviral Compounds of Phlomis viscosa Poiret.

Phlomis viscosa Poiret (an evergreen shrub) represents a valuable source of medicinal compounds. In this study, we discovered compounds with antimicrobial and antiviral properties. The aim of this study was to identify compounds of P. viscosa and estimate the antimicrobial and antiviral activity of its phytochemicals. The volatile compounds were identified using gas chromatography/mass spectrometry (GC/MS) analysis. For the identification of nonvolatile components of the extracts, high-performance liquid chromatography (HPLC), liquid chromatography-electrospray ionization-mass spectrometry (LC-ESI-MS) and matrix-assisted laser desorption/ionization-time-of-flight mass spectrometry (MALDI-TOF-MS) were applied. Quercetin 3-O-rutinoside and hesperidin caused a significant decrease in the bacterial concentration of Agrobacterium tumefaciens, Xylella fastidiosa and Pseudomonas syringae (p < 0.001). The growth of drug-resistant microorganisms (Escherichia coli, Klebsiella pneumoniae, Acinetobacter baumannii, Serratia marcescens and Salmonella enteritidis) was inhibited by quercetin 3-O-rutinoside, quercetin 3-O-arabinoside and hesperidin. In addition, these compounds demonstrated antiquorum-sensing properties. Diosmin, hesperidin and quercetin 3-O-arabinoside significantly inhibited varicella zoster virus (VZV) (p < 0.001). Quercetin 3-O-rutinoside and quercetin 3-O-arabinoside were effective against herpes simplex virus 1 (HSV-1), including mutant strains.

Cholesterol Induces Oxidative Stress, Mitochondrial Damage and Death in Hepatic Stellate Cells to Mitigate Liver Fibrosis in Mice Model of NASH.

Liver fibrosis and its end-stage disease cirrhosis are major world health problems arising from chronic injury of the liver. In recent years, the hypothesis that hepatic stellate cells' (HSCs') activation and fibrosis can be mitigated by HSC apoptosis and cell death has become of interest. In the current study, we evaluated the effect of cholesterol and bile acids on HSC apoptosis and liver fibrosis. Male C57BL/6J mice (wild type), aged four to five weeks, were fed an AIN-93G based diet (normal diet, ND), ND diet + 1% (w/w) cholesterol (CHOL group), ND diet + 0.5% (w/w) cholic acid (CA group) or ND diet + 1% (w/w) cholesterol + 0.5% (w/w) cholic acid (CHOL + CA group). Female Mdr2(-/-) mice were also treated with ND with and without 1% cholesterol. The effect of cholesterol on liver fibrosis and HSC clearance was evaluated. In addition, we studied the mechanism of cholesterol-induced apoptosis in HSC-T6 and AML-12 hepatocyte cell lines. In animals treated with cholic acids, increased lipid peroxidation and fibrosis were observed after six weeks of treatment. However, addition of cholesterol to the diet of C57BL/6J mice led to HSC-specific apoptosis and resolution of liver fibrosis, verified by double-staining with active caspase and α smooth muscle actin antibodies. In Mdr2 (-/-) mice, a diet supplemented with cholesterol corrected fibrosis and induced active hepatic stellate cells' clearance. HSC-T6 were found to be much more sensitive to cholesterol-induced oxidative stress, mitochondrial damage and apoptosis compared to hepatocytes. These results indicate that cholesterol may be a trigger of HSC lipid peroxidation and death in the liver in a model of non-alcoholic steatohepatitis. A high cholesterol-to-bile acid ratio may determine the trajectory of the liver disease toward mitigation of fibrosis.

Roseoloviruses manipulate host cell cycle.

During lytic infections HHV-6A and HHV-6B disrupt E2F1-Rb complexes by Rb degradation, releasing E2F1 and driving the infected cells toward the S-phase. Whereas upon infection E2F1 and its cofactor DP1 were up-regulated, additional E2F responsive genes were expressed differentially in various cells. E2F binding sites were identified in promoters of several HHV-6 genes, including the U27 and U79 associated with viral DNA replication, revealing high dependence on the binding site and the effect of the E2F1 transcription factor. Viral genes regulation by E2F1 can synchronize viral replication with the optimal cell cycle phase, enabling utilization of host resources for successful viral replication. Furthermore, it was found that infection by roseoloviruses leads to cell cycle arrest, mostly in the G2/M-phase.

The DR1 and DR6 first exons of human herpesvirus 6A are not required for virus replication in culture and are deleted in virus stocks that replicate well in T-cell lines.

Human herpesvirus 6A (HHV-6A) and HHV-6B are lymphotropic viruses which replicate in cultured activated cord blood mononuclear cells (CBMCs) and in T-cell lines. Viral genomes are composed of 143-kb unique (U) sequences flanked by approximately 8- to 10-kb left and right direct repeats, DR(L) and DR(R). We have recently cloned HHV-6A (U1102) into bacterial artificial chromosome (BAC) vectors, employing DNA replicative intermediates. Surprisingly, HHV-6A BACs and their parental DNAs were found to contain short approximately 2.7-kb DRs. To test whether DR shortening occurred during passaging in CBMCs or in the SupT1 T-cell line, we compared packaged DNAs from various passages. Restriction enzymes, PCR, and sequencing analyses have shown the following. (i) Early (1992) viral preparations from CBMCs contained approximately 8-kb DRs. (ii) Viruses currently propagated in SupT1 cells contained approximately 2.7-kb DRs. (iii) The deletion spans positions 60 to 5545 in DR(L), including genes encoded by DR1 through the first exon of DR6. The pac-2-pac-1 packaging signals, the DR7 open reading frame (ORF), and the DR6 second exon were not deleted. (iv) The DR(R) sequence was similarly shortened by 5.4 kb. (v) The DR1 through DR6 first exon sequences were deleted from the entire HHV-6A BACs, revealing that they were not translocated into other genome locations. (vi) When virus initially cultured in CBMCs was passaged in SupT1 cells no DR shortening occurred. (vii) Viral stocks possessing short DRs replicated efficiently, revealing the plasticity of herpesvirus genomes. We conclude that the DR deletion occurred once, producing virus with advantageous growth "conquering" the population. The DR1 gene and the first DR6 exon are not required for propagation in culture.