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The effect of cinnamaldehyde (CM) enriched diet on immunity and cytokine gene expression in Channa striatus against Aphanomyces invadans is reported. C. striatus was uniformly divided into eight groups (n = 25 fish each) and fed with formulated diets with 0, 5, 10, and 15 mg kg -1  CM enriched diet. In healthy and infected groups fed with 5 mg kg -1 diet the leukocytes count increased significantly after 4th week; with 10 mg kg -1  CM diet the increase manifested after 6th week, but with 15 mg kg -1 not even after 8th week. In both groups, 5 mg kg -1  CM diet resulted in a significant increase in the serum total protein, albumin, and globulin levels after 4th week, whereas with other diets this effect was observed only after 6th week. Similarly, with any enriched diet the lysozyme activity increased significantly, but with 15 mg kg -1  CM diet only after 6th week. In both groups the complement activity and lymphocyte production increased significantly when fed with 5 mg kg -1  CM diet after 4th week while with other enriched diets only after 6th week. The phagocytic activity increased significantly in both groups fed with 5 mg kg -1  CM diet after 6th week, whereas the SOD activity increased after 4th week. The IgM production increased significantly in both groups fed with 5 mg kg -1  CM diet after 2nd week, while with 5 and 10 mg kg -1  CM diet after 4th week. In both groups, the expression of CXCR3α was significant on 4th week when fed with 10 mg kg -1  CM diet, while in the healthy group fed with 15 mg kg -1  CM diet the expression manifested earlier than 4th week. However, when fed with 10 and 15 mg kg -1  CM diets the increase was observed on 6th week; whereas, the expression of MHC-I reached the maximum on 6th week with any enriched diet. The results indicate that in C. striatus the innate immunity and expression of cytokine and immune related genes were significantly modulated when fed with 5 mg kg -1  CM diet on 4th week against A. invadans., (Crown Copyright © 2021. Published by Elsevier Ltd. All rights reserved.)

This study aimed to investigate the effectiveness of five natural plant extract compounds Curcumin (CUR); Eugenol (EUG), Cinnamaldehyde (CIN), Stigmasterol (ST) and Morin (MOR), on two species of Saprolegnia; Saprolegnia parasitica and S. australis. Selective compounds were screened for the minimum inhibitory concentration, first for anti-oomycetes activity and then mycelium growth inhibition, spore germination inhibition and colonisation test. Nitric oxide production and myeloperoxidase activity of the compounds were tested in head kidney leukocytes of rainbow trout, Oncorhynchus mykiss to assess the immunostimulatory potential. Molecular docking of effective compounds was carried out with effector proteins of S. parasitica to investigate the target binding sites. Among all, CUR could completely inhibit zoospore production and significantly (p ≤ .05) inhibit hyphal growth at 16 mg l -1 against S. parasitica and S. australis. CIN at the concentration of 50 mg l -1 completely inhibited hyphal growth of both Saprolegnia spp., although the zoospore production of S. parasitica and S. australis was reduced at 25 mg l -1 and 10 mg l -1 . In the case of EUG, significant inhibition of the hyphal growth and germination of S. parasitica zoospores was observed at 50 mg l -1 . ST and MOR did not show antioomycetes activity. The molecular docking results were consistent with in vitro studies, possibly due to the binding with the vital proteins (Plasma membrane ATPase, V-type proton ATPase, TKL protein kinase, Host targeting protein 1) of S. parasitica and ultimately inhibiting their activity. CUR and CIN showed increased nitric oxide production at the highest concentration of 250 and 256 mg l -1 but the value was not significant (p ≤ .05) with control. CUR showed significantly higher peroxidase activity (p ≤ .05) at a concentration of 256 mg l -1 though values were significantly similar with concentration from 16 to 128 mg l -1 . The nitric oxide and total peroxidase activity of rainbow trout leukocytes in the case of CIN showed a significant difference only at 250 mg l -1 against the control. The results conclude that CUR, CIN showed the better anti-Saprolegnia activity and could be used as phyto-additives in aquaculture. Among all, the inclusion of CUR as phyto-additives will provide additional immunostimulatory activity., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

The present study was conducted to investigate the effects of dietary cinnamaldehyde nanoemulsion (CNE) on growth, digestive activities, antioxidant and immune responses and resistance against Streptococcus agalactiae (S. agalactiae) in Nile tilapia. Four experimental diets were formulated containing CNE at levels of 0, 100, 200 and 300 mg/kg diet for 12 weeks. At the end of the experiment, all fish were challenged by S. agalactiae. The results showed that the final body weight was increased in fish groups fed 200 and 300 mg CNE/kg diet by 18.4 and 17.2% with respect to the control group. Moreover, feed conversion ratio and digestive enzymes' activities were improved in groups fed 200 and 300 then 100 mg of dietary CNE/kg diet. Groups fed CNE exhibited a significant increase in serum immune-related parameters when compared with control group. Additionally, the hypocholesterolemic effects was achieved after CNE feeding unlike the control group in a dose dependent manner. With increasing dietary CNE levels, genes expression of cytokines and antioxidant enzymes were upregulated. Less severe adverse clinical symptoms and respectable cumulative mortalities associated with S. agalactiae infection were observed in fish fed CNE. To our knowledge, this study was the first offering a protective effect of CNE against S. agalactiae infection in Nile tilapia with a maximum down-regulation of cylE and hylB virulence genes expression noticed in group fed 300 mg of CNE/kg diet (up to 0.10 and 0.19- fold, respectively). Therefore, the present study recommended that an incorporation of CNE at level of 300 mg/kg diet for Nile tilapia could promote their growth, enhance their immunity and antioxidant status and provide protection against virulent S. agalactiae., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

A comparison was made between the established laser Doppler imaging (LDI) technique and the more recently developed laser speckle contrast imaging (LSCI) method to measure changes in capsaicin- and cinnamaldehyde-induced dermal blood flow (DBF) as an indicator of TRPV1 and TRPA1 activation, respectively., Methods: Capsaicin (1000 μg/20 μl) and cinnamaldehyde (10%) solutions were applied on the forearm of 16 healthy male volunteers, alongside their corresponding vehicle solutions. Pre challenge and 10, 20, 30, 40 and 60 min post challenge application, changes in DBF were assessed with the LSCI technique, followed by LDI. The area under the curve from 0 to 60 min (AUC 0 - 60 ) post capsaicin and cinnamaldehyde application was calculated as a summary measure of the response. Correlation between the LDI and LSCI instrument was assessed using a simple linear regression analysis. Sample size calculations (SSC) were performed for future studies using either the LDI or LSCI technique., Results: Higher arbitrary perfusion values were obtained with LDI compared to LSCI, yet a complete discrimination between the challenge and vehicle responses was achieved with both techniques. A strong degree of correlation was observed between LDI and LSCI measurements of the capsaicin- (R = 0.84 at Tmax and R = 0.92 for AUC 0 - 60 ) and cinnamaldehyde-induced (R = 0.78 at Tmax and R = 0.81 for AUC 0 - 60 ) increase in DBF. SSC revealed that LSCI requires considerably less subjects to obtain a power of 80% (about 15 versus 27 subjects in case of capsaicin and 7 versus 13 for cinnamaladehyde)., Conclusions: The LSCI technique was identified as the preferred method to capture capsaicin- and cinnamaldehyde-induced changes in DBF. Besides its reduced variability, the shorter scan time provides a major advantage, allowing real-time DBF measurements., Competing Interests: Declaration of competing interest The authors have no conflict of interest to declare. This research was funded by a KU Leuven Belgium Internal Fund (3M170309)., (Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.)

The objective of this study was to determine whether curcumin and a commercial microencapsulated phytogenic supplement containing thymol, cinnamaldehyde and carvacrol in broiler chicken feed would improve health and meat quality (fatty acid profile), as well as to determine the coccidiostatic and bactericidal potential of the additives. The broiler chickens were divided into five groups: NC - negative control feed; PC - positive control; CU - with 50 mg/kg of curcumin, PHY - 100 mg/kg phytogenic; and PHY + CU, a combination of both additives at 50 mg/kg (curcumin) and 100 mg/kg (phytogenic). We observed significantly higher levels of total proteins associated with increased circulating globulins, as well as lower levels of uric acid, cholesterol and triglycerides in the PHY + CU group than in the NC. There were significantly fewer oocysts in birds supplemented with additives in the NC group on day 21; on day 35, the NC, PHY and PHY + CU groups had significantly lower counts than the PC and CU groups; however, at 44 days, the lowest counts were in PC group. The bacterial counts were significantly lower on day 21 in all groups that received additives than those of the control group; however, at 44 days, the bacterial and Escherichia coli counts in these groups were significantly higher than those of the control. Curcumin with or without phytogenic agent improved meat quality, with increased antioxidant levels and reduction of lipid peroxidation. There were significantly lower total saturated fatty acid levels and significantly greater monounsaturated/polyunsaturated fatty acid levels in broilers that consumed additives individually and in combination. The combination of additives significantly increased the crypt/villus ratio, a marker of improved intestinal health and performance. Additives potentiated their individual effects, suggesting they can replace conventional growth promoters without compromising health, intestinal mucosa or meat quality., Competing Interests: Declaration of competing interest No potential conflicts of interest were reported by the authors., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

The aim of this study was to evaluate whether a phytogenic feed additive (PFA) based on essential oils such as carvacrol, thymol and cinnamic aldehyde, could be considered a replacement for antimicrobials used as growth promoters in broiler chickens, as well as to investigate its effect on total bacterial count, biochemical profiles, meat quality and meat fatty acid profile. A total of 240 broiler chicks were randomly distributed into 4 groups with 4 replicates of 15 animals each, as follow: T1 (basal diet only; the control group), T2 (basal diet supplemented with zinc bacitracin), T3 (basal diet with 0.5% of the PFA), T4 (basal diet with 1.0% of the PFA). The addition of 0.5% of the PFA improved live body weight of supplemented birds compared to the control group at 35 and 42 days of age, while the total bacterial count in the environment was reduced when 1.0% of the PFA was used. In addition, intestinal villi height and crypt depth suffered variations during the entire experiment in birds treated with both concentrations of the PFA and zinc bacitracin. Total erythrocyte counts were higher on days 14, 28 and 42 in both treated groups (PFA) compared to the control group, as well as hemoglobin content on days 28 and 42. On the other hand, leukocyte counts were lower on days 14, 28 and 42 due to reduced lymphocyte counts in both PFA treated groups compared to the control group. Serum levels of alanine aminotransferase (ALT) were lower in broilers fed with either concentration of PFA on day 14 of life, and the same was observed regarding aspartate aminotransferase (AST) in broiler treated with 0.5% of the PFA. Also, total protein and globulin levels were lower on days 14 and 28 in groups fed with phytogenic compared to the control group. Regarding meat quality, breast meat showed higher red intensity and shear force in groups fed with both concentrations of phytogenic compared to the control group, while weight loss by cooking was lower. Finally, 1.0% of phytogenic showed lower docosadienoic acid (C22:2) content in breast meat. In conclusion, results showed that the use of PFAs based on carvacrol and thymol may be considered an interesting alternative to increase broilers performance, replacing the use of antimicrobials as growth promoters, as well as an interesting alternative to reduce the total bacterial count in the environment of broiler chickens. Moreover, the diet containing phytogenic also showed hepaprotective effects but deserves attention regarding possible alterations on the immune response., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Acrolein is a highly toxic, volatile, unsaturated aldehyde generated during incomplete combustion as in tobacco smoke and indoor fires. Because the transient receptor potential ankyrin 1 (TRPA1) channel mediates tobacco smoke-induced lung injury, we assessed its role in high-level acrolein-induced toxicity in mice. Acrolein (100-275ppm, 10-30min) caused upper airway epithelial sloughing, bradypnea and oral gasping, hypothermia, cardiac depression and mortality. Male wild-type mice (WT, C57BL/6; 5-52weeks) were significantly more sensitive to high-level acrolein than age-matched, female WT mice. Both male and female TRPA1-null mice were more sensitive to acrolein-induced mortality than age- and sex-matched WT mice. Acrolein exposure increased lung weight:body weight ratios and lung albumin and decreased plasma albumin to a greater extent in TRPA1-null than in WT mice. Lung and plasma protein-acrolein adducts were not increased in acrolein-exposed TRPA1-null mice compared with WT mice. To assess TRPA1-dependent protective mechanisms, respiratory parameters were monitored by telemetry. TRPA1-null mice had a slower onset of breathing rate suppression ('respiratory braking') than WT mice suggesting TRPA1 mediates this protective response. Surprisingly, WT male mice treated either with a TRPA1 antagonist (HC030031; 200mg/kg) alone or with combined TRPA1 (100mg/kg) and TRPV1 (capsazepine, 10mg/kg) antagonists at 30min post-acrolein exposure (i.e., "real world" delay in treatment) were significantly protected from acrolein-induced mortality. These data show TRPA1 protects against high-level acrolein-induced toxicity in a sex-dependent manner. Post-exposure TRPA1 antagonism also protected against acrolein-induced mortality attesting to a complex role of TRPA1 in cardiopulmonary injury., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Short-term exposure to ambient air pollution is linked with adverse cardiovascular effects. While previous research focused primarily on particulate matter-induced responses, gaseous air pollutants also contribute to cause short-term cardiovascular effects. Mechanisms underlying such effects have not been adequately described, however the immediate nature of the response suggests involvement of irritant neural activation and downstream autonomic dysfunction. Thus, this study examines the role of TRPA1, an irritant sensory receptor found in the airways, in the cardiac response of mice to acrolein and ozone. Conscious unrestrained wild-type C57BL/6 (WT) and TRPA1 knockout (KO) mice implanted with radiotelemeters were exposed once to 3ppm acrolein, 0.3ppm ozone, or filtered air. Heart rate (HR) and electrocardiogram (ECG) were recorded continuously before, during and after exposure. Analysis of ECG morphology, incidence of arrhythmia and heart rate variability (HRV) were performed. Cardiac mechanical function was assessed using a Langendorff perfusion preparation 24h post-exposure. Acrolein exposure increased HRV independent of HR, as well as incidence of arrhythmia. Acrolein also increased left ventricular developed pressure in WT mice at 24h post-exposure. Ozone did not produce any changes in cardiac function. Neither gas produced ECG effects, changes in HRV, arrhythmogenesis, or mechanical function in KO mice. These data demonstrate that a single exposure to acrolein causes cardiac dysfunction through TRPA1 activation and autonomic imbalance characterized by a shift toward parasympathetic modulation. Furthermore, it is clear from the lack of ozone effects that although gaseous irritants are capable of eliciting immediate cardiac changes, gas concentration and properties play important roles., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Aldehydes such as acrolein are ubiquitous pollutants present in automobile exhaust, cigarette, wood, and coal smoke. Such aldehydes are also constituents of several food substances and are present in drinking water, irrigation canals, and effluents from manufacturing plants. Oral intake represents the most significant source of exposure to acrolein and related aldehydes. To study the effects of short-term oral exposure to acrolein on lipoprotein levels and metabolism, adult mice were gavage-fed 0.1 to 5 mg acrolein/kg bwt and changes in plasma lipoproteins were assessed. Changes in hepatic gene expression related to lipid metabolism and cytokines were examined by qRT-PCR analysis. Acrolein feeding did not affect body weight, blood urea nitrogen, plasma creatinine, electrolytes, cytokines or liver enzymes, but increased plasma cholesterol and triglycerides. Similar results were obtained with apoE-null mice. Plasma lipoproteins from acrolein-fed mice showed altered electrophoretic mobility on agarose gels. Chromatographic analysis revealed elevated VLDL cholesterol, phospholipids, and triglycerides levels with little change in LDL or HDL. NMR analysis indicated shifts from small to large VLDL and from large to medium-small LDL with no change in the size of HDL particles. Increased plasma VLDL was associated with a significant decrease in post-heparin plasma hepatic lipase activity and a decrease in hepatic expression of hepatic lipase. These observations suggest that oral exposure to acrolein could induce or exacerbate systemic dyslipidemia and thereby contribute to cardiovascular disease risk., (Copyright 2009 Elsevier Inc. All rights reserved.)

Acrolein is a ubiquitous environmental pollutant and an endogenous product of lipid peroxidation. It is also generated during the metabolism of several drugs and amino acids. In this study, we examined the effects of acrolein on endothelial cells. Treatment of human umbilical vein endothelial cells (HUVECs) with 2 to 10 microM acrolein led to an increase in the phosphorylation of eIF-2alpha within 10 to 30 min of exposure. This was followed by alternate splicing of XBP-1 mRNA and an increase in the expression of the endoplasmic reticulum (ER) chaperone genes Grp78 and Herp. Within 2-4 h of treatment, acrolein also increased the abundance and the nuclear transport of the transcription factors ATF3, AFT4, and CHOP. Acrolein-induced increase in ATF3 was prevented by treating the cells with the chemical chaperone - phenylbutyric acid (PBA). Treatment with acrolein increased phosphorylation of ERK1/2, p38, and JNK. The increase in JNK phosphorylation was prevented by PBA. Acrolein treatment led to activation and nuclear translocation of the transcription factor NF-kappaB and an increase in TNF-alpha, IL-6 and IL-8, but not MCP-1, mRNA. Increased expression of cytokine genes and NF-kappaB activation were not observed in cells treated with PBA. These findings suggest that exposure to acrolein induces ER stress and triggers the unfolded protein response and that NF-kappaB activation and stimulation of cytokine production by acrolein could be attributed, in part, to ER stress. Chemical chaperones of protein-folding may be useful in treating toxicological and pathological states associated with excessive acrolein exposure or production.

Formaldehyde, acetaldehyde, and acrolein are well-known upper respiratory tract irritants and occur simultaneously as pollutants in many indoor and outdoor environments. The upper respiratory tract, and especially the nose, is the prime target for inhaled aldehydes. To study possible additive or interactive effects on the nasal epithelium we carried out 1- and 3-day inhalation studies (6 hr/day) with formaldehyde (1.0, 3.2, and 6.4 ppm), acetaldehyde (750 and 1500 ppm), acrolein (0.25, 0.67, and 1.40 ppm), or mixtures of these aldehydes, using male Wistar rats and exposure concentrations varying from clearly nontoxic to toxic. The (mixtures of) aldehydes were studied for histopathological and biochemical changes in the respiratory and olfactory epithelium of the nose. In addition, cell proliferation was determined by incorporation of bromodeoxyuridine and proliferating cell nuclear antigen expression. Effects were primarily observed after 3 days of exposure. Histopathological changes and cell proliferation of the nasal epithelium induced by mixtures of the three aldehydes appeared to be more severe and more extensive in both the respiratory and the olfactory part of the nose than those observed after exposure to the individual aldehydes at comparable exposure levels. As far as nasal histopathological changes and cell proliferation are concerned neither dose addition nor potentiating interactions occurred at no-toxic-effect levels, except for a possible potentiating effect of acetaldehyde at noneffect levels. The results did not indicate a major role for aldehyde dehydrogenases in the biotransformation of the aldehydes studied. Activities of glutathione S-transferase and glutathione reductase after 3 days of exposure to acrolein, alone or in combination with formaldehyde and acetaldehyde, were depressed whereas the glutathione peroxidase activity was elevated. No decrease of nonprotein sulphydryl levels were observed. These findings suggest that, for no-toxic-effect levels, combined exposure to these aldehydes with the same target organ (nose) and exerting the same type of adverse effect (nasal cytotoxicity), but partly with different target sites (different regions of the nasal mucosa), is not associated with a greater hazard than that associated with exposure to the individual chemicals.

Biotransformation of acrolein (ACR) was studied in vivo in the rat following inhalation and ip administration. The major and minor urinary metabolites were 3-hydroxypropylmercapturic acid (HPMA) and 2-carboxyethylmercapturic acid (CEMA), respectively. Male Wistar rats were exposed to ACR, 23, 42, 77 and 126 mg/m3, for 1 hr. The sum of mercapturic acids HPMA and CEMA excreted within 24 hr after the exposure amounted to 0.87 +/- 0.12, 1.34 +/- 0.5, 2.81 +/- 1.15, and 7.13 +/- 1.56 mumol/kg, i.e., 10.9 +/- 1.5, 13.3 +/- 5.0, 16.7 +/- 6.9, and 21.5 +/- 4.8% of the estimated absorbed dose, respectively. The dose estimate was based on reported values of minute respiratory volume and respiratory tract retention and was corrected for the ACR-induced changes in minute respiratory volume. In the relevant dose range (8.9 to 35.7 mumol/kg) the portion of mercapturic acids excreted was nearly constant for ip exposed rats. The sum of HPMA and CEMA amounted to 29.1 +/- 6.5% of the dose. These results indicate that the deficiency in rat lung metabolism of ACR to acrylic acid previously observed is not compensated by the other detoxication pathway in vivo, mercapturic acid formation. The health hazard arising from inhalation of ACR is likely to be higher than that from other routes of exposure.

The goal of this study was to investigate whether coexposures to carbon black and acrolein result in a toxicologic interaction having effects on lung defenses against infectious agents. This aim was accomplished through in vivo studies with inhalation challenges of infectious agents that probe the functional integrity of the multicomponent system that comprises the integrated defenses of the lungs. Staphylococcus aureus was used for the alveolar macrophage (AM) surveillance phagocytic system, Proteus mirabilis for the dual phagocytic system composed of AMs and inflammatory polymorphonuclear leukocytes (PMNs), Listeria monocytogenes for the lymphokine-mediated arm of the acquired cellular immune response, and influenza A virus for the cytotoxic T-cell-mediated effector mechanism of cellular immunity. Exposures of Swiss mice to target concentrations of 10 mg/m3 of carbon black and 2.5 ppm acrolein for 4 hr/day for 4 days suppressed the intrapulmonary killing of S. aureus a day after exposure with a return to control levels by Day 7. In contrast, the coexposure enhanced the intrapulmonary killing of P. mirabilis which correlated with a significant increase in accessory phagocytic PMNs recovered from the lungs. Combined exposure to carbon black and acrolein also resulted in impaired elimination of L. monocytogenes and influenza A virus from the lungs. Neither exposure to carbon black alone nor exposure to acrolein alone had any effect on the functional integrity of lung defenses against the four infectious agents. These data demonstrate the effects of the toxicologic interaction of coexposures to an inert particle and acrolein on innate and acquired defenses of the lungs. The mechanism for the enhanced biologic effect may be that the carbon black particle acts as a carrier mechanism for acrolein to the deep lung.