Review Article: Oral malodour and active ingredients for treatment

Oral care preparations are widely used for the treatment of oral malodour as over‐the‐counter products. Bad breath is highly distressing to an individual’s confidence during social interaction, which is a large concern nowadays as the consumption of these products is increasing worldwide. However, oral deodorant ingredients are rarely studied compared with other cosmetic ingredients, and the only preparations which are well known are those contained in dentifrices and mouthrinses. This review briefly summarizes the compounds which cause oral malodour and the treatments available. The active ingredients in various preparations are emphasized and novel products are presented.     

Deodorants and antiperspirants: New trends in their active agents and testing methods

Sweating is the human body's thermoregulation system but also results in unpleasant body odour which can diminish the self-confidence of people. There has been continued research in finding solutions to reduce both sweating and body odour. Sweating is a result of increased sweat flow and malodour results from certain bacteria and ecological factors such as eating habits. Research on deodorant development focuses on inhibiting the growth of malodour-forming bacteria using antimicrobial agents, whereas research on antiperspirant synthesis focuses on technologies reducing the sweat flow, which not only reduces body odour but also improves people's appearance. Antiperspirant's technology is based on the use of aluminium salts which can form a gel plug at sweat pores, obstructing the sweat fluid from arising onto the skin surface. In this paper, we perform a systematic review on the recent progress in the development of novel antiperspirant and deodorant active ingredients that are alcohol-free, paraben-free, and naturally derived. Several studies have been reported on the alternative class of actives that can potentially be used for antiperspirant and body odour treatment including deodorizing fabric, bacterial, and plant extracts. However, a significant challenge is to understand how the gel-plugs of antiperspirant actives are formed in sweat pores and how to deliver long-lasting antiperspirant and deodorant benefits.     

Iron sequestration on skin: a new route to improved deodorancy

Axillary malodour is caused by the biotransformation of non-odorous precursors present in apocrine sweat and sebum by the axillary microflora. To counter this, underarm products typically contain high levels of bactericides. However, after an initial decrease in bacterial numbers, the surviving cells grow, producing a concomitant rise in axillary odour. A sustained deodorant effect might be achieved without recourse to bactericidal action if this bacterial growth could be inhibited for extended periods. The current study attempted to inhibit axillary bacterial growth by nutrient deprivation, primarily that of iron (Fe(III)). In vitro analyses identified iron (Fe(III)) as the trace metal whose deprivation had the most profound effect on bacterial growth. Further in vitro investigations with Fe-chelating agents demonstrated that a number of compounds with high binding constants for Fe(III) showed optimal activity. One candidate molecule, diethylenetriaminepentaacetic acid (DTPA), was capable of effectively inhibiting bacterial growth in vitro and on the skin of the lower back. Some bacterial species could additionally utilize iron bound to the iron carrier protein transferrin present in eccrine sweat. This was minimized by the use of an agent, butylated hydroxytoluene (BHT), capable of liberating iron from transferrin via reduction of transferrin-bound ferric ions, allowing subsequent sequestration of Fe(II). Deodorant efficacy evaluation of the combination of DTPA and BHT showed deodorancy benefits over and above that afforded by DTPA alone. This mixture of DTPA and BHT supplemented to a standard ethanolic deodorant, used on 50 people for 2 weeks, was highly effective in limiting bacterial growth in the axilla. Total aerobic bacteria in the axillae were reduced from a mean of log 5.75 (+/-0.73) to log 4.50 (+/-0.90) colony-forming units (cfu) cm(-2) (n = 27, P < 0.01) compared with a non-fortified standard ethanolic deodorant. This was reflected in significant decreases in axillary malodour production, as determined by malodour assessments (P < 0.01). The profile of the axillary microflora was maintained, and all populations were rapidly returned to preuse levels after cessation of product use. This new deodorant technology was benchmarked against leading antimicrobial-based deodorant systems. In three separate deodorant efficacy evaluations, the combination of DTPA and BHT was tested against Triethyl citrate, Triclosan and Farnesol in standard unfragranced ethanolic formulations. The combination of DTPA and BHT showed highly significant deodorancy benefits over and above all these antimicrobial-based deodorant technologies. The combination of an efficient iron chelator with an agent capable of liberating iron from transferrin offers significant benefits in terms of bacterial growth inhibition on the skin and provides a new route to axillary deodorancy.     

The evaluation of underarm deodorants

Double-blind cross-over trials in which trained assessors evaluated axillary malodour on a 0 to 10 scale showed that ethanol at 60% and 99% w/w significantly reduced odour for up to 24 h. Reduction in odour was increased by the addition of non-volatile antimicrobial ingredients such as chlorhexidine, Irgasan DP 300 (Triclosan, Ciba Geigy) or aluminium chlorhydrate.
Volunteer panellists were able to identify statistically significant deodorant effects when they rated their own axillary odour on a 0 to 10 scale.
An odour absorber, zinc ricinoleate (Grillocin, Grillo-Werke, A. G.) was used to treat existing malodour and gave reduced perception of that malodour for up to 24 h.
A close correlation was found between panel odour scores and the bacterial status of the axilla as assessed by the replipad technique when biocidal systems were studied. Irgasan DP 300, a bacteriostat, did not perform so well in skin flora sampling procedures, but was nevertheless effective as a deodorant ingredient. Thus in vivo microbiological techniques, although often useful as predictors of deodorancy, do not replace the carefully controlled clinical trial with direct assessment of odour.
L'evaluation de l'odeur des aisselles     

Generation of volatile fatty acids by axillary bacteria

It is generally accepted that short-chain (C(2)-C(5)) volatile fatty acids (VFAs) are among the causal molecules of axillary malodour. It is also widely acknowledged that malodour generation is attributable to the biotransformation of odourless natural secretions, into volatile odorous products, by axillary bacteria. However, little information is available on the biochemical origins of VFAs on axillary skin. In these studies, assay systems were developed to investigate the generation of VFAs from substrates readily available to the bacteria resident on axillary skin. Propionibacteria and staphylococci were shown to ferment glycerol and lactic acid to the short-chain (C(2)-C(3)) VFAs, acetic and propionic acid. Furthermore, staphylococci are capable of converting branched aliphatic amino acids, such as leucine, to highly odorous short-chain (C(4)-C(5)) methyl-branched VFAs, such as isovaleric acid, which are traditionally associated with the acidic note of axillary malodour. However, in vitro kinetic data indicates that these pathways contribute less to axillary VFA levels, than fatty acid biotransformations by a recently defined sub-group of the Corynebacterium genus, corynebacteria (A). The results of these studies provide new understanding on the biochemical origins of VFA-based axillary malodour which, in turn, should lead to the development of novel deodorant systems.     

Methionine restriction up‐regulates the expression of the pi class of glutathione S‐transferase partially via the extracellular signal‐regulated kinase‐activator protein‐1 signaling pathway initiated by glutathione depletion

Understanding the molecular events underlying gene regulation by amino acids has attracted increasing attention. Here, we explored whether the mechanism by which methionine restriction affects the expression of the π class of glutathione S‐transferase (GSTP) is related to oxidative stress initiated by glutathione (GSH) depletion. Rat primary hepatocytes were cultured in an L‐15‐based medium in the absence or presence of 200 μM L ‐buthionine sulfoximine (BSO) or in a methionine‐restricted L‐15 medium supplemented with 20 μM L ‐methionine up to 72 h. BSO and methionine restriction time‐dependently induced GSTP mRNA and protein expression in a similar pattern accompanied by a decrease in the cellular GSH level. The phosphorylation of extracellular signal‐regulated kinase (ERK), but not of c‐Jun NH₂‐terminal kinase and p38, was stimulated by methionine restriction and BSO. Electromobility gel shift assay showed that the DNA‐binding activity of nuclear activator protein‐1 (AP‐1) increased in cells exposed to methionine restriction or BSO. With the ERK inhibitor FR180204, AP‐1 activation and GSTP expression were abolished. Moreover, the induction of GSTP by methionine restriction and BSO was reversed by GSH monoethyl ester and N‐acetylcysteine. Our results suggest that methionine restriction up‐regulates GSTP gene expression, which appears to be initiated by the ERK‐AP‐1 signaling pathway through GSH depletion in rat hepatocytes.     

应用男体出汗图谱的运动装设计与性能评价

运动装的结构设计影响其热湿传递性能,从而影响着装者的舒适性。本研究根据男体局部出汗分布特征和当前各种吸湿排汗面料的特性,设计不同面料拼接的几款运动装,采用34区段出汗暖体假人‘Newton’来客观评价所研发的人体绘图运动服装（Body Mapping Sportswear）的热阻、湿阻和透湿指数,并通过热应激预测（PHS）模型预测在各种环境条件下穿着运动装后的人体生理指标（包括皮肤温度、核心温度、出汗率、总出汗量）变化,从而评价所研制的运动装在不同环境下对人体的热调节作用。     

Suppression of EGF-induced tumor cell migration and matrix metalloproteinase-9 expression by capsaicin via the inhibition of EGFR-mediated FAK/Akt, PKC/Raf/ERK, p38 MAPK, and AP-1 signaling

Scope: Capsaicin is a cancer‐suppressing agent. The aim of our study was to determine the effect of capsaicin on tumor invasion and migration; the possible mechanisms involved in this inhibition were investigated in human fibrosarcoma cells. Methods and results: We employed invasion, migration and gelatin zymography assays to characterize the effect of capsaicin on HT‐1080 cells. Transient transfection assays and immunoblot analysis were performed to study its molecular mechanisms of action. Capsaicin inhibited the epidermal growth factor (EGF)‐induced activation of matrix metalloproteinase (MMP)‐9 and MMP‐2, and further inhibited cell invasion and migration. Capsaicin decreased the EGF‐induced expression of MMP‐9, MMP‐2, and MT1‐MMP, but did not alter TIMP‐1 and TIMP‐2 levels. Capsaicin suppressed EGF‐induced c‐Jun and c‐Fos nuclear translocation, and also abrogated the EGF‐induced phosphorylation of EGF receptor (EGFR), focal adhesion kinase (FAK), protein kinase C (PKC), phosphatidylinositol 3‐Kinase (PI3K)/Akt, extracellular regulated kinase (ERK)1/2, and JNK1/2, an upstream modulator of AP‐1. Furthermore, the EGFR inhibitor inhibited EGF‐induced MMP‐9 expression, as well as AP‐1 activity and cell migration. Conclusion: Capsaicin inhibited the EGF‐induced invasion and migration of human fibrosarcoma cells via EGFR‐dependent FAK/Akt, PKC/Raf/ERK, p38 mitogen‐activated protein kinase (MAPK), and AP‐1 signaling, leading to the down‐regulation of MMP‐9 expression. These results indicate the role of capsaicin as a potent anti‐metastatic agent, which can markedly inhibit the metastatic and invasive capacity of fibrosarcoma cells.     

The suppressive effect of apricot kernel extract on 5alpha-Androst-16-en-3-one generated by microbial metabolism

Body odours are generated from dead skin cells and secreted materials, such as sweat and sebum, through the metabolism of microorganisms living on the skin. Volatile steroids, key compounds in body odours, are also generated through the metabolism of microorganisms. These volatile steroids strengthen the intensity of the overall body malodour and are sensed differently by males and females. Females are more sensitive than males to volatile steroids, especially 5alpha-androst-16-en-3-one (androstenone). To regulate body odours that are especially unpleasant for women, we devised an androstenone-generation model using the metabolism of Corynebacterium xerosis, which is one of the bacteria living on the axillary skin. Using this model, we studied the suppressive effect of plant extracts on the generation of androstenone. We found that apricot kernel extract (AKE) had the most positive effect among the plant extracts to which we applied the model. However, although AKE did suppress androstenone generation, it did not show any bactericidal effect. Using the cell-free system, AKE also suppressed the generation of androstenone. In conclusion, we found that AKE suppressed the generation of androstenone, which is especially unpleasant for women, and the mechanism was not bactericidal but metabolic inhibition. The results of these studies provide new understanding of the regulation of androstenone, which, in turn, should lead to the development of novel deodorant systems.     

Protective effects of enzymatic digest from Ecklonia cava against high glucose‐induced oxidative stress in human umbilical vein endothelial cells

BACKGROUND: Antioxidants can prevent pathological damage caused by hyperglycaemia‐induced oxidative stress associated with diabetes. In the present study, we investigated whether the brown alga Ecklonia cava has protective effects against high glucose‐induced oxidative stress in Human umbilical vein endothelial cells (HUVECs). For that purpose, we prepared an enzymatic digest from E. cava (ECC) by using the carbohydrase, Celluclast. RESULTS: High glucose treatment induced HUVECs cell death, but ECC, at a concentration of 10 or 100 µg mL^?1, significantly inhibited the high glucose‐induced cytotoxicity. Furthermore, treatment with ECC dose‐dependently decreased thiobarbituric acid reactive substances (TBARS), intracellular generation of reactive oxygen species, and the nitric oxide level increased by high glucose. In addition, ECC treatment increased activities of antioxidant enzymes including catalase, superoxide dismutase and glutathione peroxidase in high‐glucose pretreated HUVECs. High glucose levels induced the overexpression of inducible nitric oxide synthase, cyclooxygenase‐2 and nuclear factor‐kappa B proteins in HUVECs, but ECC treatment reduced the overexpression of these proteins. CONCLUSION: These results suggest that ECC is a potential therapeutic agent that will reduce the damage caused by hyperglycaemia‐induced oxidative stress associated with diabetes. Copyright © 2009 Society of Chemical Industry     

Oxidized proteins and their biological impact

Aging is characterized by an increased accumulation of damaged macromolecules and oxidized protein build up is considered to be a hallmark of cellular aging. Advanced glycation end products (AGE) have been analyzed in aging human peripheral blood lymphocytes since such glycoxidative modifications have been reported to increase with age in a variety of cellular and tissular systems and are believed to contribute to the intracellular age‐related accumulation of damaged proteins, a process that has been associated with the cellular functional deficits that occur with age. The pattern of glycated protein has been studied using two dimensional gel electrophoresis followed by Western blotting with an anti‐AGE antibody. The protein silver stain and the immunoblot patterns were not superimposable indicating that glycoxidative modifications are targeting only a restricted set of proteins. Among these preferential protein targets, seven of them exhibited a significant age‐related increased immunoreactivity with the anti‐AGE antibody suggesting that the corresponding modified proteins might serve as biomarkers of aging lymphocytes [ 1 ]. Other age‐related protein modifications such as carbonyl formation and conjugation with the lipid peroxidation product 4‐hydroxy‐2‐nonenal are also currently studied. The age‐related accumulation of altered protein raises the problem of the efficacy of intracellular protein maintenance, in particular the protein degradation and the protein repair systems. Indeed, if these systems that take care of the removal or repair of damaged proteins are affected with aging, they would therefore directly contribute to the increased intracellular load of functionally impaired protein. Since cytosolic oxidized protein degradation and basal protein turnover have been shown to be mostly carried out by the proteasomal system, the fate of proteasome in aging has been addressed and a decline of proteasomal proteolytic activity has been reported [ 2 ]. The impact of aging on human lymphocyte 26S proteasome has been recently investigated and age‐related alterations of proteasome structure and function have been evidenced. Indeed, we observed a decline of 26S proteasome specific activity which is correlated to an increasing yield of post‐translational modifications of proteasome subunits [ 3 ]. In fact, some proteasome subunits and particularly assembly and catalytic subunits are specifically modified with age. According to bidimensional westernblotting, some subunits were found either glycated, conjugated with the lipid peroxidation product 4‐hydroxy‐2‐nonenal or even ubiquitinated. In vitro treatment of the proteasome by glyoxal, that promotes the formation of N?‐carboxymethyllysine adducts, or by the lipid peroxidation product 4‐hydroxy‐2‐nonenal was found to inactivate its peptidase activities although to different extent. In other studies aimed at monitoring the effect of oxidative stress on proteasome structure and function, we have shown on an in vivo rat model that coronary occlusion/reperfusion resulted in inactivation of the proteasome [ 4 ]. This inactivation is associated with selective modification by the lipid peroxidation product 4‐hydroxy‐2‐nonenal of three 20S proteasome α‐subunits. In contrast, the observed inhibition of proteasome upon exposure of human keratinocytes to UV stress was mainly due to the stress‐induced formation of endogeneous inhibitors, including certain oxidatively modified proteins [ 5 ]. In addition, the role of the peptide methionine sulfoxide reductase, one of the very few protein repair enzyme described, and its possible implication in the age‐related decline of protein maintenance has been investigated. The peptide methionine sulfoxide reductase system (Msr A and Msr B) catalyzes the reduction of methionine sulfoxide to methionine within proteins and its activity and the expression of Msr A have been shown to decline in different organs of aged rats [ 6 ] and more recently in senescent human fibroblasts. Moreover, we have recently shown that the peptide methionine sulfoxide reductase Msr A is present both in the cytosol and in the mitochondrial matrix, although under different isoforms [ 7 ]. In conclusion, during aging or in certain oxidative stress situations, impairment of both peptide methionine sulfoxide reductases and proteasome activity appears as a critical factor in the decreased efficacy of intracellular protein maintenance, contributing to the increased intracellular load of modified and functionally impaired proteins that may ultimately lead to a global deterioration of cellular homeostasis.     

Characterization of the microflora of the human axilla

It is widely accepted that axillary malodour is attributable to the microbial biotransformation of odourless, natural secretions into volatile odorous products. Consequently, there is a need to understand the microbial ecology of the axilla in order that deodorant products, which control microbial action in this region, can be developed in the appropriate manner. A detailed characterization of the axillary microflora of a group of human volunteers has been performed. The axillary microflora is composed of four principal groups of bacteria (staphylococci, aerobic coryneforms, micrococci and propionibacteria), and the yeast genus Malassezia. Results indicated that the axillary microflora was dominated by either staphylococcal or aerobic coryneform species. Comparisons between axillary bacterial numbers and levels of axillary odour demonstrated the greatest association between odour levels and the presence of aerobic coryneforms in the under-arm. As the taxonomy of cutaneous aerobic coryneforms is poorly understood, a further study was conducted to characterize selected axillary aerobic coryneform isolates. Using the molecular technique of 16S rDNA sequencing, selected genomic sequences of a number of axillary aerobic coryneform isolates were obtained. Comparisons with sequence databases indicated the likely presence of a range of Corynebacterium species on axillary skin, although the majority of isolates were most similar to either Corynebacterium G-2 CDC G5840 or C. mucifaciens DMMZ 2278. Although for a panel of individuals differences in the carriage of Corynebacterium species were noted, similar species were carried by a number of panellists. All isolates examined in this limited evaluation failed to demonstrate the capability to metabolize long-chain fatty acids (LCFAs) to shorter chain, more volatile products. The application of this modern molecular phylogenetic technique has increased understanding of the diversity of aerobic coryneform carriage in the axilla, and on human skin. The application of this technique in other studies to assess the ethnic differences in cutaneous bacterial ecology, or the effects on the microflora of specific product use, will assist in the future development of novel deodorant systems.     

Apocynin exerts neuroprotective effects in fumonisin b1–induced neurotoxicity via attenuation of oxidative stress and apoptosis in an animal model

The Fusarium verticillioides produces a mycotoxin, that is, fumonisin b1 (Fb1), which commonly infects corn and agricultural commodities. The Fb1 showed hepatotoxicity, neurotoxicity, and carcinogenicity in animals. Hence, the present investigation aimed to evaluate the effect of apocynin (AP) on Fb1-induced neurotoxic effects and its mechanism in the mice model and cell line. The male Balb/c mice, with the 6.75 mg/kg bwt of Fb1 were injected subcutaneously for 5 days to induce neurotoxicity. A significant elevation of serotonin (5-HT) was observed in mice treated with Fb1 in the whole brain showing biogenic amines may reflect Fb1 neurotoxicity, but the negatively regulated mechanisms were attenuated by the pretreatment of AP. In addition, AP pretreatment normalized apoptotic changes in histology and immunohistochemistry studies. In Western blotting studies, apoptotic genes were upregulated and oxidative stress genes were downregulated due to Fb1 treatment; while treating with AP, these gene expressions were rectified. Further cell cytotoxicity was investigated by MTT and lactate dehydrogenase (LDH) assays in SH-SY5Y cell line. MTT and LDH assays indicated the IC₅₀ value to be 150 µM of Fb1, which was protected by 100 µg of AP. The electron microscopy evaluated the Fb1-induced apoptotic conditions and its cell morphology recovery by AP. These results suggest that nicotinamide adenine dinucleotide phosphate hydrogen oxidase–mediated reactive oxygen species is the primary upstream signal leading to increased Fb1-mediated neurotoxicity in mice. The use of the antioxidant AP reversed the toxin-induced oxidative stress and apoptosis by its antioxidant potency.     

Skin ageing: changes of physical properties of human skin in vivo

We have investigated in vivo the change with age of various parameters that describe the physical properties of skin. The parameters were derived from pressure/displacement curves obtained by applying reduced pressure to a small area of skin and measuring the resulting displacement by 20 MHz scan echography. By fitting the pressure/displacement curves to a theoretical model, the following skin parameters were obtained: E, Young's modulus or stiffness (in Pascals); sigma(0), the initial stress (in Pascals); and the unrestored energy ratio (UER), an index related to cutaneous non-elasticity. These parameters, which are used in mechanics to define the intrinsic physical characteristics of materials, were measured for the first time on volar forearm skin of 206 male and female subjects, aged between 6 months and 90 years. The results showed that skin thickness increases until maturity and decreases for women over 50-60 years old, Young's modulus E increases linearly with age, and ageing is divided into two phases for natural stress, sigma(0) and the non-elasticity index UER. Natural stress sigma(0) increases until maturity and then rapidly decreases. The non-elasticity index decreases until puberty and steadily increases after puberty. This new procedure provides a simple quantitative assessment of the physical properties of the skin, revealing that the skin becomes thinner, stiffer, less tense and elastic with ageing.     

Comparison of Gender Differences in Nutritional Value and Key Odor Profile of Hepatopancreas of Chinese Mitten Crab (Eriocheir Sinensis)

The nutritional value and key odor profile of hepatopancreas of Chinese mitten crab (Eriocheir sinensis) was evaluated, and gender differences in terms of edible yield, proximate composition, different lipid fractions, fatty acid composition, and key odor compounds were compared. Total lipids were separated into different lipid fractions using silicic acid columns. And odorants were detected by monolithic material sorptive extraction coupled with gas chromatography‐mass spectrometry‐olfactometry (GC‐MS‐O). Furthermore, detected frequency and odor intensity method of GC‐O were applied to select key odor compounds in steamed E. sinensis. The results showed male crabs (34.06%) had a higher edible yield than female crabs (32.42%). Hepatopancreas was the most abundant portion in both genders, which contained high lipid content. Higher contents of triacylglycerols, sterols, free fatty acids, and phosphatidylethanolamine in female crabs resulted in a significant higher total lipid content in females (40.05%) than in males (37.94%). Meanwhile, total monounsaturated fatty acids and polyunsaturated fatty acids of female crabs had significant higher content than male crabs, and the ratio of docosahexaenoic acid to eicosapentaenoic acid of female crabs (1.26) showed higher value than male crabs (1.18), which indicated that female crabs had higher nutritional value than male crabs. For further analyses, unique odor compounds detected in female crabs showed a plant/vegetable‐like odor, while sweety, corn‐like odor in male crabs. These suggested that hepatopancreases of female crabs are healthier than male crabs for human consumption, however, they may be favored by different consumers individually due to their unique aroma profiles.     

Imprinted gene expression in the rat embryo-fetal axis is altered in response to periconceptional maternal low protein diet

In our previous study, we have shown that maternal low protein diet (LPD, 9% casein vs 18% casein control) fed exclusively during the rat preimplantation period (0-4.25 day postcoitum) induced low birth weight, altered postnatal growth and hypertension in a gender-specific manner. In this study, we investigated the effect of maternal LPD restricted only to the preimplantation period (switched diet) or provided throughout gestation on fetal growth and imprinted gene expression in blastocyst and fetal stages of development. Male, but not female, blastocysts collected from LPD dams displayed a significant reduction (30%) in H19 mRNA level. A significant reduction in H19 (9.4%) and Igf2 (10.9%) mRNA was also observed in male, but not in female, fetal liver at day 20 postcoitum in response to maternal LPD restricted to the preimplantation period. No effect on the blastocyst expression of Igf2R was observed in relation to maternal diet. The reduction in H19 mRNA expression did not correlate with an observed alteration in DNA methylation at the H19 differentially methylated region in fetal liver. In contrast, maternal LPD throughout 20 days of gestation did not affect male or female H19 and Igf2 imprinted gene expression in fetal liver. Neither LPD nor switched diet treatments affected H19 and Igf2 imprinted gene expression in day 20 placenta. Our findings demonstrate that one contributor to the alteration in postnatal growth induced by periconceptional maternal LPD may derive from a gender-specific programming of imprinted gene expression originating within the preimplantation embryo itself.     

不同日龄、性别、部位Hyla兔系肌内脂肪酸组成变化

以Hyla配套系肉兔为对象,研究不同日龄、性别、部位Hyla兔系肌内脂肪酸组成的动态变化,探讨肉兔生长过程中脂肪酸的沉积规律及营养价值。结果表明：随着日龄的增加,Hyla公兔和母兔背部最长肌（longissimus dorsi,LD）、左后腿肌（left-hind leg muscle,LL）和腹肌（abdominal muscle,AM）的肌内总脂肪含量均显著增加（P＜0.05）,且AM中含量最高,LL次之,LD最低,公兔整体低于母兔;经气相色谱分析,共鉴定出21 种脂肪酸,其中不饱和脂肪酸（unsaturated fatty acids,UFA）的含量丰富,尤其是长链（C20～22）多不饱和脂肪酸（polyunsaturated fatty acids,PUFA）;随着Hyla兔的生长,3 个部位肌内脂肪的PUFA/SFA值、n-6 PUFA含量及n-3 PUFA含量显著下降（P＜0.05）,n-6/n-3值因日龄、性别和部位的差异有着不同的动态变化,比值范围为6.5～8.5;经偏最小二乘回归分析可知,日龄、性别与部位均能够显著影响Hyla兔系肌内脂肪酸组成,其中,幼龄公兔LL脂肪酸组成更优,而成年母兔LD更适宜加工。     

Curcumin induces heme oxygenase-1 in normal human skin fibroblasts through redox signaling: relevance for anti-aging intervention

Scope: Curcumin, a component of the spice turmeric, was tested for its potential hormetic anti‐aging effects as an inducer of mild stress. Methods and results: Early passage young human skin fibroblasts treated with low doses of curcumin (below 20 μM) showed a time‐ and concentration‐dependent induction of heme oxygenase‐1 (HO‐1), followed by compensatory increase in glutathione‐S‐transferase activity, GSH levels and GSH/GSSG ratio. These effects were preceded by induction of oxidative stress (increased levels of reactive oxygen species and DNA damage) and impairment of cells' GSH redox state. Curcumin also induced nuclear factor‐erythroid‐2‐related factor 2 accumulation in the nuclei. The use of the antioxidant N‐acetyl cysteine prevented the induction of HO‐1 by curcumin. Pharmacological inhibition of phosphatidylinositol 3‐kinase, but not other kinases, significantly prevented curcumin‐induced HO‐1 levels, which was corroborated by the induction of phospho‐Akt levels by curcumin. Late passage senescent cells already had higher HO‐1 levels, and further induction of HO‐1 by curcumin was considerably impaired. The induction of stress responses by curcumin in human cells led to protective hormetic effects to further oxidant challenge. Conclusion: Curcumin induces cellular stress responses in normal human skin fibroblasts through phosphatidylinositol 3‐kinase/Akt pathway and redox signaling, supporting the view that curcumin‐induced hormetic stimulation of cellular antioxidant defenses can be a useful approach toward anti‐aging intervention.