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The electronic cigarettes (e-cigarettes, e-cigs) have become the most sought-after alternative to the traditional cigarettes, partly due to the widespread perception of safety. However, the high temperature reached by e-cig solutions can generate toxic compounds, some of which are listed as known human carcinogens. To evaluate the impact of e-cig aerosol on rat brain lipid profile, twenty male Sprague Dawley rats were exposed to 11 cycles/day (E-cig group), to consume 1 mL/day of e-liquid, for 5 days/week up to 8 weeks. Ten rats were sacrificed after 4 weeks (4w) and ten at the end of treatment (8w). The composition of total fatty acids, sterols and oxysterols of the lipid fraction of rat brains, was analyzed. The results of the E-cig group were compared with those of the control group (not exposed). After 8 weeks, the saturated fatty acids significantly raised up to 7.35 mg/g tissue, whereas polyunsaturated fatty acids decreased reaching 3.17 mg/g. The e-cig vaping increased both palmitic (3.43 mg/g) and stearic acids (3.82 mg/g), while a significant decrement of arachidonic (1.32 mg/g) and docosahexaenoic acids (1.00 mg/g) was found. Atherogenic (0.5) and thrombogenic (1.12) indices also increased in 8w treated animals. The e-cig aerosol significantly impacted the cholesterol homeostasis, since the latter at 8w (21.57 mg/g) was significantly lower than control (24.56 mg/g); moreover, a significant increase of 7-dehydrocholesterol (1.87 mg/g) was also denoted in e-cig group. The e-cig aerosol also reduced the oxysterol formation (19.55 μg/g) after 4 weeks of exposure, except for triol and 5α,6α-epoxycholesterol (α-EC). The principal component analysis (PCA) separated all E-cig from control groups, evidencing that oxysterols (except triol and 24(S)-hydroxycholesterol (24(S)-HC)) were inversely correlated to 7-DHC and TI. The present research revealed that e-cigs aerosol affected the lipid and cholesterol homeostasis in rat brain, which could contribute to the new occurrence of some neurodegenerative diseases.

Sulforaphane (SFN) and moringin (GMG-ITC) are edible isothiocyanates present as glucosinolate precursors in cruciferous vegetables and in the plant Moringa oleifera respectively, and recognized for their chemopreventive and medicinal properties. In contrast to the well-studied SFN, little is known about the molecular pathways targeted by GMG-ITC. We investigated the ability of GMG-ITC to inhibit essential signaling pathways that are frequently upregulated in cancer and immune disorders, such as JAK/STAT and NF-kappa B. We report for the first time that, similarly to SFN, GMG-ITC in the nanomolar range suppresses IL-3-induced expression of STAT5 target genes. GMG-ITC, like SFN, does not inhibit STAT5 phosphorylation, suggesting a downstream inhibitory event. Interestingly, treatment with GMG-ITC or SFN had a limited inhibitory effect on IFN alpha-induced STAT1 and STAT2 activity, indicating that both isothiocyanates differentially target JAK/STAT signaling pathways. Furthermore, we showed that GMG-ITC in the micromolar range is a more potent inhibitor of TNF-induced NF-kappa B activity than SFN. Finally, using a cellular system mimicking constitutive active STAT5-induced cell transformation, we demonstrated that SFN can reverse the survival and growth advantage mediated by oncogenic STAT5 and triggers cell death, therefore providing experimental evidence of a cancer chemopreventive activity of SFN. This work thus identified STAT5, and to a lesser extent STAT1/STAT2, as novel targets of moringin. It also contributes to a better understanding of the biological activities of the dietary isothiocyanates GMG-ITC and SFN and further supports their apparent beneficial role in the prevention of chronic illnesses such as cancer, inflammatory diseases and immune disorders.

Electronic cigarettes (e-cigs) are devices designed to deliver nicotine in a vaping solution rather than smoke and without tobacco combustion. Perceived as a safer alternative to conventional cigarettes, e-cigs are aggressively marketed as lifestyle-choice consumables, thanks to few restrictions and a lack of regulatory guidelines. E-cigs have also gained popularity among never-smokers and teenagers, becoming an emergent public health issue. Despite the burgeoning worldwide consumption of e-cigs, their safety remains largely unproven and it is unknown whether these devices cause in vivo toxicological effects that could contribute to cancer. Here we demonstrate the co-mutagenic and cancer-initiating effects of e-cig vapour in a rat lung model. We found that e-cigs have a powerful booster effect on phase-I carcinogen-bioactivating enzymes, including activators of polycyclic aromatic hydrocarbons (PAHs), and increase oxygen free radical production and DNA oxidation to 8-hydroxy-2'-deoxyguanosine. Furthermore, we found that e-cigs damage DNA not only at chromosomal level in peripheral blood, such as strand breaks in leucocytes and micronuclei formation in reticulocytes, but also at gene level such as point mutations in urine. Our results demonstrate that exposure to e-cigs could endanger human health, particularly among younger more vulnerable consumers.

Introduction: Obesity is recognized as a leading global health concern, associated with an increased risk for several chronic diseases. The brain plays a key role in energy homeostasis as the master regulator of food intake balance and energy expenditure, controlling the adipose mass gain responding to hormonal and nutrient-related signals. Promising weigh-management strategies include the use of vegetables rich in bioactive compounds, to improve the antioxidant status and to stimulate lipid catabolism. The aim of this study was to evaluate the dietary effects of Raphanus sativus cv Sango on lipid accumulation and oxysterols in brain of obese rats. Materials and Methods: Four-day old Raphanus sativus cv Sango sprouts (SSJ) were squeezed to obtain a juice, which was collected and used for the experiments. Thirty-five male Sprague Dawley rats aged 9 weeks (270–300 g), after 10-days adaptation, were split randomly into five groups (7 animals per group) and fed specific diets: RD-RD (regular diet for 14 weeks); HFD-HFD (high fat diet for 14 weeks); HFD-RD (HFD for 10 weeks and then RD for 4 weeks); HFD-RD 75 (HFD for 10 weeks and then RD and 75 mg/kg b.w. SSJ for 4 weeks); HFD-HFD 75 (HFD for 10 weeks and then HFD and 75 mg/kg b.w. SSJ for 4 weeks). After 14 weeks, rats’ brains were isolated and their lipid matter was subjected to the analysis of total fatty acids, sterols and oxysterols composition. Results: The lipid content, fatty acid composition, cholesterol and its oxidation products (COPs) content were significantly affected. The HFD-HFD group showed a fat accumulation in the brain, with a significant reduction of linoleic acid. Although the lowest cholesterol content was detected on HFD-HFD group, the latter generated the highest COPs amount (63.098 microg/g brain). The main COPs foundwere 7alfa/beta-hydroxycholesterol, alfa/beta-epoxycholesterols, 7-ketocholesterol, cholestanetriol and 24-hydroxycholesterol. The Principal Component Analysis revealed that all COPs were highly correlated to HFD-HFD diet, except for 24-hydroxycholesterol which resulted highly correlated to linoleic acid content. Conclusions: The high fat diet increased lipid infiltration in rat brain, however, it reduced the amount of cholesterol with a significant increase of COPs, except for 24-hydroxycholesterol, thus confirming the inflammatory status. However, the Raphanus sativus cv Sango sprouts supplementation was not able to counteract the oxidative stress in rat brain since the lipidomic profile was not significantly affected.

Objectives We used acetylsalicylic acid (ASA) as a probing agent to quantify hydroxyl radical (·OH) in Controls and patients with coronary artery disease and to prospectively investigate ·OH production in patients with myocardial infarction (MI) complicated by heart failure (HF). Background Oxidative stress status (OSS) is a mechanism for transition to HF in experimental heart injury models, but evidence for its causal role in humans is still limited. Methods Thirty healthy subjects (Controls), 12 patients with stable angina (Group 1), and 74 patients with ST-segment elevation MI (Group 2) were enrolled. A dose of 250 mg Flectadol was given intravenously before each blood collection to determine the 2,3-dihydroxybenzoic acid/salicylic acid (DHBA/SA) ratio. We also quantified vitamin E and coenzyme Q10to monitor antioxidant reserve, as well as tumor necrosis factor (TNF)-alpha, TNF-soluble receptors, interleukin (IL)-6, and IL-1ra to assess inflammatory status. All measurements were repeated at month 6 in Group 2. Results There were no differences between Controls and Group 1. Group 2 showed increased ·OH production, peaking at 24 h, whereas vitamin E and coenzyme Q10progressively declined. Group 2 patients developing HF during hospitalization (Group 2Bi) presented with an increase of both ·OH production at discharge and inflammatory status, as compared with patients without HF (Group 2Ai), persisting at month 6 in post-MI patients with HF (Group 2Bii). Conclusions We found a distinct pattern of ·OH generation in post-MI patients who show progression to HF. The interplay between OSS and inflammatory status should be targeted as a possible mechanism of progression to post-MI left ventricular dysfunction.