Cashew nut allergy: clinical relevance and allergen characterisation

Cashew plant (Anacardium occidentale L.) is the most relevant species of the Anacardium genus. It presents high economic value since it is widely used in human nutrition and in several industrial applications. Cashew nut is a well-appreciated food (belongs to the tree nut group), being widely consumed as snacks and in processed foods by the majority of world's population. However, cashew nut is also classified as a potent allergenic food known to be responsible for triggering severe and systemic immune reactions (e.g. anaphylaxis) in sensitised/allergic individuals that often demand epinephrine treatment and hospitalisation. So far, three groups of allergenic proteins have been identified and characterised in cashew nut: Ana o 1 and Ana o 2 (cupin superfamily) and Ana o 3 (prolamin superfamily), which are all classified as major allergens. The prevalence of cashew nut allergy seems to be rising in industrialised countries with the increasing consumption of this nut. There is still no cure for cashew nut allergy, as well as for other food allergies; thus, the allergic patients are advised to eliminate it from their diets. Accordingly, when carefully choosing processed foods that are commercially available, the allergic consumers have to rely on proper food labelling. In this sense, the control of labelling compliance is much needed, which has prompted the development of proficient analytical methods for allergen analysis. In the recent years, significant research advances in cashew nut allergy have been accomplished, which are highlighted and discussed in this review.This work was supported by FCT/MEC through national funds and co-financed by FEDER, under the Partnership Agreement PT2020 with grant no. UID/QUI/50006/2013–POCI/01/ 0145/FEDER/007265. Joana Costa is grateful to FCT post-doctoral grant (SFRH/BPD/102404/2014) financed by POPH-QREN (subsidised by FSE and MCTES).info:eu-repo/semantics/publishedVersio

Effect of blood nitrite and nitrate levels on murine platelet function.

Nitric oxide (NO) appears to play an important role in the regulation of thrombosis and hemostasis by inhibiting platelet function. The discovery of NO generation by reduction of nitrite (NO₂⁻) and nitrate (NO₃⁻) in mammals has led to increased attention to these anions with respect to potential beneficial effects in cardiovascular diseases. We have previously shown that nitrite anions at 0.1 µM inhibit aggregation and activation of human platelet preparations in vitro in the presence of red blood cells and this effect was enhanced by deoxygenation, an effect likely due to NO generation. In the present study, we hypothesized that nitrite and nitrate derived from the diet could also alter platelet function upon their conversion to NO in vivo. To manipulate the levels of nitrite and nitrate in mouse blood, we used antibiotics, NOS inhibitors, low nitrite/nitrate (NOx) diets, endothelial NOS knock-out mice and also supplementation with high levels of nitrite or nitrate in the drinking water. We found that all of these perturbations affected nitrite and nitrate levels but that the lowest whole blood values were obtained by dietary restriction. Platelet aggregation and ATP release were measured in whole blood and the results show an inverse correlation between nitrite/nitrate levels and platelet activity in aggregation and ATP release. Furthermore, we demonstrated that nitrite-supplemented group has a prolonged bleeding time compared with control or low NOx diet group. These results show that diet restriction contributes greatly to blood nitrite and nitrate levels and that platelet reactivity can be significantly affected by these manipulations. Our study suggests that endogenous levels of nitrite and nitrate may be used as a biomarker for predicting platelet function and that dietary manipulation may affect thrombotic processes

Effect of nitrite and nitrate supplementation on the levels of nitrite and nitrate in whole blood.

<p>C57BL/6 mice were divided into three groups. Control group received normal water (no treatment), second group received nitrite (0.1 g/L)-containing water and the third group received nitrate (1 g/L)-containing water for a week. All groups were fed standard diets during the treatment period. Nitrite (A) and nitrate (B) in the whole blood from each group were measured using a chemiluminescence NO analyzer (Sievers, Model 280 NO analyzer). Data are means ± SEM (n≥4). * p<0.05.</p

Influences of different perturbations in NO metabolism on nitrite and nitrate levels in whole blood.

<p>C57BL/6 mice were randomly divided into four groups and treated with antibiotics (bacitracin (4 mg/ml), neomycin (4 mg/ml), tetracycline (1 mg/ml)) or L-NAME (1 g/L) or low nitrite/nitrate (NOx) diet for a week. Age-matched eNOS knock-out mice were used. Nitrite (A) and nitrate (B) were measured using a chemiluminescence NO analyzer (Sievers, Model 280 NO analyzer). Relative values to wild-type control on standard diets were calculated in each treatment group and inserted in both (A) and (B). Data are means ± SEM (n≥7). *p<0.05.</p

Effect of nitrite and nitrate supplementation on platelet reactivity in whole blood.

<p>Whole blood from the control (no treatment) mice or the mice that were given additional nitrite (0.1 g/L) or nitrate (1 g/L) in the drinking water for a week was taken and diluted with saline (1∶4) for aggregation (A and B) and ATP release (C) measurement. Chronolume® was added to the diluted blood for 2 min at 37°C for ATP measurement and then platelets were activated by collagen (0.5∼3 µg/ml) addition. Aggregation amplitude was shown as maximal impedance (A) and the total response duration was expressed as area under the 5-min aggregation curve (AUC, B). The amount of ATP released from platelets was analyzed by luciferin-luciferase assay using an ATP standard (C). Control (no treatment): open diamond, nitrite (0.1 g/L): red square, nitrate (1 g/L): blue triangle. Data are means ± SEM (n≥5). * p<0.05 compared with control (no treatment) at each concentration of collagen.</p

Measurement of tail bleeding time.

<p>Mice were divided into three groups for 1-week treatment; control (no treatment, standard diets), nitrite supplementation (0.1 g/L) and low NOx diet group. Nitrite in the whole blood from each group of mice was measured using a chemiluminescence NO analyzer (A) (Sievers, Model 280 NO analyzer). The tail was amputated 0.5 cm from the tip and blood was blotted onto filter paper every 10 seconds (B). Data are means ± SEM (n≥8). *p<0.05.</p

Dietary Inorganic Nitrate as an Ergogenic Aid: An Expert Consensus Derived via the Modified Delphi Technique.

INTRODUCTION: Dietary inorganic nitrate is a popular nutritional supplement, which increases nitric oxide bioavailability and may improve exercise performance. Despite over a decade of research into the effects of dietary nitrate supplementation during exercise there is currently no expert consensus on how, when and for whom this compound could be recommended as an ergogenic aid. Moreover, there is no consensus on the safe administration of dietary nitrate as an ergogenic aid. This study aimed to address these research gaps. METHODS: The modified Delphi technique was used to establish the views of 12 expert panel members on the use of dietary nitrate as an ergogenic aid. Over three iterative rounds (two via questionnaire and one via videoconferencing), the expert panel members voted on 222 statements relating to dietary nitrate as an ergogenic aid. Consensus was reached when > 80% of the panel provided the same answer (i.e. yes or no). Statements for which > 80% of the panel cast a vote of insufficient evidence were categorised as such and removed from further voting. These statements were subsequently used to identify directions for future research. RESULTS: The 12 panel members contributed to voting in all three rounds. A total of 39 statements (17.6%) reached consensus across the three rounds (20 yes, 19 no). In round one, 21 statements reached consensus (11 yes, 10 no). In round two, seven further statements reached consensus (4 yes, 3 no). In round three, an additional 11 statements reached consensus (5 yes, 6 no). The panel agreed that there was insufficient evidence for 134 (60.4%) of the statements, and were unable to agree on the outcome of the remaining statements. CONCLUSIONS: This study provides information on the current expert consensus on dietary nitrate, which may be of value to athletes, coaches, practitioners and researchers. The effects of dietary nitrate appear to be diminished in individuals with a higher aerobic fitness (peak oxygen consumption [V̇O2peak] > 60 ml/kg/min), and therefore, aerobic fitness should be taken into account when considering use of dietary nitrate as an ergogenic aid. It is recommended that athletes looking to benefit from dietary nitrate supplementation should consume 8-16 mmol nitrate acutely or 4-16 mmol/day nitrate chronically (with the final dose ingested 2-4 h pre-exercise) to maximise ergogenic effects, taking into consideration that, from a safety perspective, athletes may be best advised to increase their intake of nitrate via vegetables and vegetable juices. Acute nitrate supplementation up to ~ 16 mmol is believed to be safe, although the safety of chronic nitrate supplementation requires further investigation. The expert panel agreed that there was insufficient evidence for most of the appraised statements, highlighting the need for future research in this area