BACKGROUND:

Genetic and nutritional factors play an important role in inflammatory response and diseases. CXCL10 is a critical biomarker that is involved in multiple inflammatory diseases, and elevated levels of CXCL10 have been associated with the development of several chronic and infectious diseases. In contrast, micronutrients can attenuate inflammatory responses. Single nucleotide polymorphisms in the pro-inflammatory cytokine genes such as IL-1β at rs16944 contributed to a number of inflammatory disorders and may substantiate the convergance between chronic and infectious diseases.

AIM:

This study aims to identify the modifying effect of nutritional factors on the association between IL-1β genotypes and CXCL10 levels.

METHODS:

Participants (N = 386) were healthy males and females from the Toronto Nutrigenomics and Health study recruited from the University of Toronto. Levels of micronutrients and inflammatory markers were measured in plasma. IL-1β genotypes were extracted from the Affymetrix 6.0 SNP chip.

RESULTS:

CXCL10 levels were not different across different IL-1β genotypes. Among those with the GA genotype, elevated CXCL10 levels were observed with higher than median ascorbic acid (β = 0.004 ± 0.002, P = 0.047) or higher than median vitamin D status (β = 0.003 ± 0.002, P = 0.044). Among participants with the AA genotype, subjects with low α-tocopherol status had elevated levels of CXCL10 (β = -0.016 ± 0.007, P = 0.012).

CONCLUSION:

The association between IL-1β rs16944 genotype and CXCL10 levels was modified by the levels of ascorbic acid, α-tocopherol and vitamin D. These findings may aid in understanding the combined effect of genetic and dietary factors in the development of various infectious and chronic diseases in which IL-1β and CXCL10 may play an etiological role.

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Glutathione peroxidase 4 (GPx4) is a unique antioxidant enzyme that directly reduces the phospholipid hydroperoxides (PLOOH) generated in biomembranes using glutathione as the reductant. We have previously reported that the Caenorhabditis elegans gpx-quad mutant, which lacks all homologous genes of GPx4 has a reduced lifespan compared with the wild-type. However, the mechanisms underlying the lifespan reduction remain unclear. By monitoring the change in PLOOH production with age, we found that PLOOH was elevated in the gpx-quad mutants compared with the wild-type during the reproductive period. Administration of vitamin E not only reduced the PLOOH content but also prolonged the lifespan of the gpx-quad mutants. In contrast, vitamin C did not extend the lifespan of the gpx-quad mutants. Interestingly, we found that the inhibition of lipid peroxidation by vitamin E during 5 to 10 days after hatching is important to extend the lifespan of C. elegans. These results suggest that production of PLOOH during the reproductive period strongly influences the lifespan of C. elegans.

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Fipronil (FIP) is a highly effective, broad-use insecticide that belongs to the phenylpyrazole chemical group. It is extensively used in the agriculture and veterinary medicine for controlling a wide variety of pests. Though FIP showed lower toxicity in vertebrates than in insects, it was recognized to have a variety of toxic effects in mammals. The present study was undertaken to evaluate FIP-induced alterations in the blood biochemical markers and oxidative stress parameters in male albino mice via oral sub-acute toxicity exposure. The possible ameliorative effect of the pretreatment with selenium plus α-tocopherol (vitamin E) against the harmful effects of FIP was also investigated. Mice in FIP-test groups were exposed to different sublethal doses, i.e., 1.43, 2.87, and 4.78 mg active ingredient (AI)/kg body weight (b.w.), equal to 1/100, 1/50, and 1/30 LD₅₀ of FIP, respectively, for 28 days. Mice in the amelioration groups were orally administered with selenium + vitamin E (0.3 mg + 22.5 mg/kg b.w., respectively) 14 days prior to exposure to the higher dose (4.78 mg/kg) of FIP for another 14 days. Fipronil exposure at medium and high doses showed lowered values of red blood cell count (RBC), hematocrit (HCT), hemoglobin (HGB), white blood cell (WBC), and platelet (PLT) counts after 28-day exposure, compared to the control. All three doses caused significant increases in levels of liver-function biomarkers, i.e., aspartate amino transaminase (AST), alanine amino transaminase (ALT), alkaline phosphatase (ALP), cholesterol, and bilirubin levels compared to the control. Levels of biomarkers related to kidney functions, i.e., urea, uric acid, and creatinine, increased significantly than these of the control. Likewise, the oxidative stress indices, i.e., hydrogen peroxide (H₂O₂) and malondialdehyde (MDA), significantly increased at the higher and medium doses, while antioxidant enzymes, catalase (CAT) and superoxide dismutase (SOD), decreased significantly. On the other hand, prior administration of selenium + vitamin E in the FIP-exposed mice led to restore values of most hematological parameters nearly to these of the control. Also, the levels of AST, total protein, and creatinine seemed to be restored to the control values. Interestingly, pretreatment with selenium + vitamin E restored the levels of antioxidant enzymes, CAT and SOD, to the control values, whereas, oxidative stress indices, H₂O₂ and MDA, remained significantly high. It is our thought that the sublethal dose less than 1.43 mg/kg b.w. of commercial formulation of FIP (COACH^® 200 SC) could be considered as no-observed-adverse-effect-level(NOAEL) under our present experimental conditions at short-term toxicity study. On the other hand, the higher sublethal doses, 4.78 and 2.87 mg/kg b.w., induced significant adverse effects in biomarkers and may be deleterious to human health following long-term exposure.

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In the present study, modified extraction methods using supercritical CO₂ were investigated in order to obtain high-added value compounds from rapeseed oil deodorizer distillate and comparisons were done with modified Soxhlet extraction (solvent extraction + silica). For supercritical fluid extraction (SFE), the optimal extraction parameters were temperature of 40 °C, pressure of 350 bar (for phytosterols), 400 bar (for tocopherol), 5 wt% ethanol as co-solvent, and saponification pretreatment. The optimized SFE procedure led to the recovery of three main phytosterols (50 wt % β-sitosterol, 23.91 wt % Brassicasterol, and 36.25 wt % Campesterol) and only α-tocopherol. Moreover, there was no synergistic effect with saponification pretreatment + co-solvent and the efficiency and concentration of target compounds were less than supercritical CO₂ + co-solvent. Also, comparative Data showed that the efficiency of phytosterols and tocopherols was approximately three times higher (p < 0.05) in SFE relative to modified Soxhlet extraction. Furthermore, the use of ethanol (5 wt %) as co-solvent, improved phytosterols and tocopherol efficiency and purity. The SFE technique offers various advantages over the modified Soxhlet extraction technique, including increasing the solubility of tocopherols and sterols by using CO₂+ co-solvent, minimized usage of toxic organic solvents and increased purity of extracted products.

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This study aimed to examine whether the oral supplementation of vitamins C and E during a seven-day high salt diet (HS; ~14 g salt/day) prevents microvascular endothelial function impairment and changes oxidative status caused by HS diet in 51 (26 women and 25 men) young healthy individuals. Laser Doppler flowmetry measurements demonstrated that skin post-occlusive reactive hyperemia (PORH), and acetylcholine-induced dilation (AChID) were significantly impaired in the HS group, but not in HS+C+E group, while sodium nitroprusside-induced dilation remained unaffected by treatments. Serum oxidative stress markers: Thiobarbituric acid reactive substances (TBARS), 8-iso prostaglandin-F2α, and leukocytes’ intracellular hydrogen peroxide (H₂O₂) production were significantly increased, while ferric-reducing ability of plasma (FRAP) and catalase concentrations were decreased in the HS group. All these parameters remained unaffected by vitamins supplementation. Matrix metalloproteinase 9, antioxidant enzymes Cu/Zn SOD and glutathione peroxidase 1, and leukocytes’ intracellular superoxide production remained unchanged after the protocols in both HS and HS+C+E groups. Importantly, multiple regression analysis revealed that FRAP was the most powerful predictor of AChID, while PORH was strongly predicted by both FRAP and renin-angiotensin system activity. Hereby, we demonstrated that oxidative dis-balance has the pivotal role in HS diet-induced impairment of endothelial and microvascular function in healthy individuals which could be prevented by antioxidative vitamins consumption.

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OBJECTIVE:

This study aims to analyze the presence of oxidative stress and activity of the antioxidant system in the parotid and submandibular salivary glands of rats with Chronic Kidney Disease (CKD).

DESIGN:

Sixteen male wistar rats were divided into two groups (n = 8, each): control rats and rats with CKD. CKD was induced by 5/6 nephrectomy. Blood urea nitrogen and serum creatinine clearance were quantified. Malondialdehyde, superoxide dismutase, glutathione peroxidase, glutathione reductase, catalase, total antioxidant status, ascorbic acid, α-tocopherol, superoxide anion, and hydrogen peroxide concentrations were assessed.

RESULTS:

In CKD rats, blood urea nitrogen, serum creatinine, and proteinuria concentrations were increased, while creatinine clearance was reduced. In the submandibular gland, superoxide anion concentration was increased significantly (p < 0.05). Hydrogen peroxide and superoxide anion concentrations were reduced in the parotid gland. CKD rats presented increased malondialdehyde concentration, total antioxidant status, superoxide dismutase, and glutathione reductase activities only in the parotid gland (p < 0.05).

CONCLUSION:

Oxidative stress and changes in the antioxidant system were found in the parotid and submandibular salivary glands in an experimental model of CKD induced by 5/6 nephrectomy.

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The aim of this study is the analysis of the in vitro digestion of corn oil, and of the effect of its enrichment with three levels of gamma– and alpha-tocopherol, by using, for the first time, ¹H nuclear magnetic resonance (¹H NMR) and a solid phase microextraction followed by gas chromatography/mass spectrometry (SPME-GC/MS). The attention is focused on the hydrolysis degree, the degradation of oil’s main components, the occurrence of oxidation reactions and main compounds formed, as well as on the bioaccessibility of oil’s main components, of compounds formed in the oxidation, and, of gamma– and alpha-tocopherol. The lipolysis levels reached are high and show a similar pattern in all cases. The oxidation of corn oil components during in vitro digestion is proven, as is the action of gamma-tocopherol as an antioxidant and alpha-tocopherol as a prooxidant. In the more alpha-tocopherol enriched samples, hydroperoxy-, hydroxy-, and keto-dienes, as well as keto-epoxy-monoenes and aldehydes, are generated. The bioaccessibility of the oil’s main components is high. The compounds formed in the oxidation process during in vitro digestion can also be considered bioaccessible. The bioaccessibility of alpha-tocopherol is smaller than that of gamma-tocopherol. The concentration of this latter compound remains unchanged during the in vitro digestion of the more alpha-tocopherol enriched oil samples.

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Tree nuts and peanuts are healthful foods with a track record of helping to reduce the incidence of chronic diseases, most notably cardiovascular disease. At the point of consumption, all nuts contain low moisture and ≥ 50% lipid contents, but this is where similarities end. The levels of key nutrients and bioactives including vitamin C, vitamin E, L-arginine, minerals (such as selenium and zinc), and phenolics differ. Distinctions in the types and quantities of phenolic constituents for tree nut species as well as the impact of digestion will affect the nuts’ antioxidant potential in vivo. This chapter provides some insight into the different types of phenolics found in tree nuts and peanuts, the antioxidant potential of phenolic extracts using in vitro chemical assays, the effect of thermal processing on the stability of the nuts’ endogenous phenolics, and the impact on biomarkers of human health arising from randomized clinical trials. Key biomarkers include measures in the reduction of LDL oxidation as well as increases in the levels of vitamin E and selected phenolic compounds in blood plasma postprandially from those of baseline.

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Recent findings implied the significance of reactive oxygen species (ROS) as a part of tyrosine kinase inhibitors (TKIs) pharmacological activity. Evidences also suggested that toxic effects of TKIs were related to ROS production. The results regarding benefits of vitamin E usage alongside with prescribed TKIs therapy are ambiguous. We aimed to examine oxidative stress and antioxidative defense in human serum treated with four different TKIs and their possible interactions with hydrosoluble vitamin E analog (Trolox). An in-vitro experiment with serum pool as a substitute model was performed. Different parameters of oxidative stress and antioxidative defense were measured in serum pool with and without addition of TKIs (axitinib, crizotinib, nilotinib, and imatinib), before and after addition of Trolox. Z score statistic was used for calculation of Prooxidative and Antioxidative scores. The highest oxidative potential was recorded for samples incubated with imatinib and nilotinib, while the lowest damaging scores were observed for crizotinib and axitinib (nilotinib vs. imatinib, P < 0.05; axitinib vs. imatinib, P < 0.01; crizotinib vs. imatinib, P < 0.001). The best capability for antioxidative protection was seen in samples with nilotinib, then with imatinib, while the lowest level was obtained in samples with crizotinib and axitinib (imatinib and axitinib vs. nilotinib, P < 0.05 for both; crizotinib vs. nilotinib, P < 0.01; axitinib vs. imatinib, P < 0.05, crizotinib vs. imatinib, P < 0.01). Our results demonstrated the opposite effects of Trolox in combination with imatinib and nilotinib. Usage of antioxidant in combination with TKIs should be carefully evaluated in each specific case.

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