PMID: 

Metallomics. 2014 Mar ;6(3):662-71. Epub 2014 Feb 19. PMID: 24549367

Abstract Title: 

Mechanisms of Hg species induced toxicity in cultured human astrocytes: genotoxicity and DNA-damage response.

Abstract: 

The toxicologically most relevant mercury (Hg) species for human exposure is methylmercury (MeHg). Thiomersal is a common preservative used in some vaccine formulations. The aim of this study is to get further mechanistic insight into the yet not fully understood neurotoxic modes of action of organic Hg species. Mercury species investigated include MeHgCl and thiomersal. Additionally HgCl2 was studied, since in the brain mercuric Hg can be formed by dealkylation of the organic species. As a cellular system astrocytes were used. In vivo astrocytes provide the environment necessary for neuronal function. In the present study, cytotoxic effects of the respective mercuricals increased with rising alkylation level and correlated with their cellular bioavailability. Further experiments revealed for all species at subcytotoxic concentrations no induction of DNA strand breaks, whereas all species massively increased H2O2-induced DNA strand breaks. This co-genotoxic effect is likely due to a disturbance of the cellular DNA damage response. Thus, at nanomolar, sub-cytotoxic concentrations, all three mercury species strongly disturbed poly(ADP-ribosyl)ation, a signalling reaction induced by DNA strand breaks. Interestingly, the molecular mechanism behind this inhibition seems to be different for the species. Since chronic PARP-1 inhibition is also discussed to sacrifice neurogenesis and learning abilities, further experiments on neurons and in vivo studies could be helpful to clarify whether the inhibition of poly(ADP-ribosyl)ation contributes to organic Hg induced neurotoxicity.

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PMID: 

Nutr Res. 2019 May 23 ;68:19-33. Epub 2019 May 23. PMID: 31252376

Abstract Title: 

Phenolic-enriched raspberry fruit extract (Rubus idaeus) resulted in lower weight gain, increased ambulatory activity, and elevated hepatic lipoprotein lipase and heme oxygenase-1 expression in male mice fed a high-fat diet.

Abstract: 

Red raspberries (Rubus idaeus) contain numerous phenolic compounds with purported health benefits. Raspberry ketone (4-(4-hydroxyphenyl)-2-butanone) is a primary raspberry flavor phenolic found in raspberries and is designated as a synthetic flavoring agent by the Food and Drug Administration. Synthetic raspberry ketone has been demonstrated to result in weight loss in rodents. We tested whether phenolic-enriched raspberry extracts, compared with raspberry ketone, would be more resilient to the metabolic alterations caused by an obesogenic diet. Male C57BL/6J mice (8 weeks old) received a daily oral dose of vehicle (VEH; 50% propylene glycol, 40% water, and 10% dimethyl sulfoxide), raspberry extract low (REL; 0.2 g/kg), raspberry extract high (REH; 2 g/kg), or raspberry ketone (RK; 0.2 g/kg). Coincident with daily dosing, mice were placed on a high-fatdiet (45% fat). After 4 weeks, REH and RK reduced body weight gain (approximately 5%-9%) and white adipose mass (approximately 20%) compared with VEH. Hepatic gene expression of heme oxygenase-1 and lipoprotein lipase was upregulated in REH compared with VEH. Indirect calorimetry indicated that respiratory exchange ratio (COproduction to Oconsumption) was lower, suggesting increased fat oxidation with all treatments. REH treatment increased total ambulatory behavior. Energy expenditure/lean mass was higher in REH compared with REL treatment. There were no treatment differences in cumulative intake, meal patterns, or hypothalamic feed-related gene expression. Our results suggest that raspberry ketone and a phenolic-enriched raspberry extract both have the capacity to prevent weight gain but differ in the preventative mechanisms for excess fat accumulation following high-fat diet exposure.

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The chemical war against cholesterol using statin drugs has been wrongly justified through statistical deception and the ongoing cover up of over 300 adverse health effects documented in the biomedical literature.

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Originally Published On ElectricSense.com

Is there a connection between cell phones and cancer?  Here are 44 reasons to believe that cell phones can cause cancer.

Cell phones emit microwave radio-frequency radiation. Fact.

This radiation has the ability to penetrate our bodies. Fact.

Our governments do virtually nothing to protect us from these dangers. Fact.

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PMID: 

Mol Nutr Food Res. 2019 03 ;63(5):e1800985. Epub 2018 Dec 13. PMID: 30521111

Abstract Title: 

Dietary Prevention of Colitis by Aronia Berry is Mediated Through Increased Th17 and Treg.

Abstract: 

SCOPE: Increased fruit consumption is associated with reduced risk of colitis. It has been investigated whether the anti-colitic effects of the polyphenol-rich aronia berry (Aronia mitschurinii 'Viking') are mediated through Th17 and Treg.METHODS AND RESULTS: Colitis is induced in recombinase activating gene-1 deficient mice injected with syngeneic CD4CD62Lnaïve T cells. Mice consume either 4.5% w/w aronia-berry-supplemented or a control diet concurrent with T cell transfer. The extent of colitis and immunocyte populations are evaluated at weeks 3 to 7 after transfer. Aronia consumption prevents colitic wasting and reduces colon weight/length ratios relative to the control diet at weeks 5 and 7. Compared to the control diet, aronia feeding increases Treg in mesenteric lymph node at all colitis stages. Treg and regulatory Th17 subpopulations (IL-17AIL-10and IL-17AIL-22) are increased in lamina propria and spleen at week 5 in aronia-fed mice. Aronia feeding also decreases total CD4cells but increases colonic Tregs. The ability of aronia to modulate colonic cytokines is associated with functional T cell IL-10 and increased diversity of microbiota.CONCLUSIONS: Aronia berry consumption inhibits adoptive transfer colitis by increasing Treg and regulatory Th17 cells. Dietary modulation of T cells is dynamic and precedes colitic wasting.

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PMID: 

Nutrients. 2019 May 24 ;11(5). Epub 2019 May 24. PMID: 31137670

Abstract Title: 

Activity-Guided Fractionation of Red Fruit Extracts for the Identification of Compounds Influencing Glucose Metabolism.

Abstract: 

An activity-guided search for compounds influencing glucose metabolism in extracts from aronia (, A.), pomegranate (, P.), and red grape () was carried out. The three extracts were fractionated by means of membrane chromatography to separate the anthocyanins from other noncolored phenolic compounds (copigments). In addition, precipitation with hexane was performed to isolate the polymers (PF). The anthocyanin and copigment fractions (AF, CF) of aronia, pomegranate, and red grape were furthermore fractionated with high-performance countercurrent chromatography (HPCCC) and the subfractions were characterized by HPLC-PDA-MS/MS analyses. Each of the (sub-)fractions was examined by in vitro-tests, i.e., the inhibition of the activity ofα-amylase and α-glucosidase. On the basis of this screening, several potent inhibitors of the two enzymes could be identified, which included flavonols (e.g., quercetin), ellagitannins (e.g., pedunculagin), and anthocyanins (e.g., delphinidin-3-glucoside and petunidin-3-glucoside). In the α-glucosidase assay all of the examined fractions and subfractions of the fruit extracts were more active than the positive control acarbose.

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PMID: 

J Agric Food Chem. 2019 Jul 10 ;67(27):7726-7737. Epub 2019 Jun 25. PMID: 31203627

Abstract Title: 

Polyphenol-Rich Loquat Fruit Extract Prevents Fructose-Induced Nonalcoholic Fatty Liver Disease by Modulating Glycometabolism, Lipometabolism, Oxidative Stress, Inflammation, Intestinal Barrier, and Gut Microbiota in Mice.

Abstract: 

Fructose as a daily sweetener is widely recognized as a risk catalyst for nonalcoholic fatty liver disease (NAFLD). The aim of current study is to evaluate the effects and molecular mechanism by which polyphenol-rich loquat fruit extract (LFP) prevents NAFLD in mice fed 30% fructose water (HF) for 8 weeks. Administration of LFP to HF-fed mice mitigated abnormal body weight, disordered lipid metabolism, oxidative stress, and inflammation through a mechanism regulated by the AKT, ChREBP/SREBP-1c, Nrf2, and TLR4/MyD88/TRIF pathways. LFP caused a significant decrease in the endotoxin content (16.67-12.7 EU/mL) in the liver of HF-fed mice. LFP not only improved HF-induced breakage of the intestinal barrier via interacting with tight junction proteins (ZO-1, occludin), mucin, and immunoreaction in the colon but also maintained normal colonic/ratios and the relative abundance ofin HF-fed mice. Our results suggest that LFP may serve as a nutritional agent for protecting liver in HF-fed mice.

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PMID: 

Zhongguo Zhong Yao Za Zhi. 2019 Feb ;44(4):774-780. PMID: 30989891

Abstract Title: 

[Protective effect of raspberry extract on ConA-induced acute liver injuryin mice].

Abstract: 

In this experiment,the antioxidant capacity of raspberry extract and the protective effect on liver injury induced by ConA in mice were investigated. Balb/C male mice were randomly divided into six groups: normal group,model group,bicyclol control group( 200 mg·kg~(-1)),low-dose raspberry extract group( 200 mg·kg~(-1)),middle-dose raspberry extract group( 400 mg·kg~(-1)),and highdose raspberry extract group( 800 mg·kg~(-1)). Each group was intragastrically administered with drugs according to the body weight once a day. Seven days later,all of the groups except for the normal group were treated with ConA( 20 mg·kg~(-1)) through tail vein injection to establish the acute liver injury model. The mice were put to death 8 hours later. The organ indexes were calculated. These rum levels of ALT,AST and LDH and the activities of SOD,CAT,GSH and MDA inliver tissue were detected. HE staining was used to observe the pathological changes of liver tissue in mice. Western blot was used to detect the expressions of Bax,Bcl-2,Nrf2 and Keap-1. The antioxidant capacity of raspberry extract was measured by CAA assay. The results showed that,raspberry extract had a strong antioxidant capacity. Simultaneously,compared with the model group,raspberry extract can significantly improve the pathological conditions of liver,and significantly reduce ALT,AST and LDH activities in serum of liver injury mice( P

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PMID: 

BMC Complement Altern Med. 2019 Jun 20 ;19(1):140. Epub 2019 Jun 20. PMID: 31221152

Abstract Title: 

Neutralization of cholera toxin by Rosaceae family plant extracts.

Abstract: 

BACKGROUND: Cholera is one of the most deadly diarrheal diseases that require new treatments. We investigated the neutralization of cholera toxin by five plant extracts obtained from the Rosaceae family that have been traditionally used in Poland to treat diarrhea (of unknown origin).METHODS: Hot water extracts were prepared from the dried plant materials and lyophilized before phytochemical analysis and assessment of antimicrobial activity using microdilution assays. The ability of the plant extracts to neutralize cholera toxin was analyzed by measurement of cAMP levels in cell cultures, enzyme-linked immunosorbent assay and electrophoresis, as well as flow cytometry and fluorescence microscopy studies of fluorescent-labeled cholera toxins with cultured human fibroblasts.RESULTS: The antimicrobial assays displayed modest bacteriostatic potentials. We found that the plant extracts modulate the effects of cholera toxin on intracellular cAMP levels. Three plant extracts (Agrimonia eupatoria L., Rubus fruticosus L., Fragaria vesca L.) suppressed the binding of subunit B of cholera toxin to the cell surface and immobilized ganglioside GMwhile two others (Rubus idaeus L., Rosa.canina L.) interfered with the toxin internalization process.CONCLUSIONS: The traditional application of the Rosaceae plant infusions for diarrhea appears relevant to cholera, slowing the growth of pathogenic bacteria and either inhibiting the binding of cholera toxin to receptors or blocking toxin internalization. The analyzed plant extracts are potential complements to standard antibiotic treatment and Oral Rehydration Therapy for the treatment of cholera.

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PMID: 

Exp Physiol. 2019 Jul 11. Epub 2019 Jul 11. PMID: 31297904

Abstract Title: 

Rosa canina L. methanolic extract prevents heat stress-induced memory dysfunction in rats.

Abstract: 

NEW FINDINGS: What is the central question of this study? Heat stress has harmful effects on the brain structure and synaptic density via induction of oxidative stress and neuroinflammation, which result in neuronal damage in the hippocampus and thereby cognitive impairments. In this study, we investigate the effect of Rosa canina treatment on cognitive function in heat stress-exposed rats and its underlying mechanisms. What is the main finding and its importance? We show that R. canina improves cognitive deficits induced by heat stress by attenuation of oxidative stress and neuroinflammation and by upregulation of synaptic proteins in the hippocampus.ABSTRACT: The aim of the study was to evaluate the effects of aqueous methanolic extract of Rosa canina (RC) dried fruits on oxidative stress, inflammation, synaptic degeneration and memory dysfunction induced by heat stress (HS) in rats. Sixty adult male Wistar rats were randomly divided into five groups as follows: the control group received normal saline (NS); the HS group was exposed to heat stress (43°C) for 15 min once a day for 2 weeks; and HS+R groups were exposed to heat stress and received one of three doses (250, 500 or 1000 mg kg) of RC methanolic extract for 2 weeks. A passive avoidance test and a Y-maze test were performed to assess learning and memory. The levels of reactive oxygen species were assessed. The serum cortisol concentration and hippocampal total antioxidant capacity, superoxide dismutase and glutathione peroxidase were also detected usingspectrophotometry. The protein expressions of c-Fos, heat-shock protein-70, tumour necrosis factor-α, growth-associated protein 43, post-synaptic density-95 and synaptophysin were evaluated in the hippocampal tissue. The results showed that RC significantly improved cognitive dysfunction inducedby HS, which was accompanied by downregulation of tumour necrosis factor-α and upregulation of growth-associated protein 43 and synaptophysin proteins in the hippocampus of HS-exposed rats. Furthermore, RC significantly attenuated serum cortisol concentrations and upregulated heat shock protein-70and c-Fos in the hippocampus. In addition, the administration of RC attenuated reactive oxygen species levels and enhanced antioxidant defense in the hippocampus. These findings indicate that RC attenuated the deleterious effect of HS on cognition through its antioxidant properties and by enhancingsynaptic function and plasticity.

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