Removal of anionic and cationic dyes using porous chitosan/carboxymethyl cellulose-PEG hydrogels: Optimization, adsorption kinetics, isotherm and thermodynamics studies.

Chitosan (CS)/carboxymethyl cellulose (CMC) porous hydrogels chemically crosslinked by epichlorohydrin were synthesized using polyethylene glycol (PEG) as a pore-forming agent for anionic (Congo red, CR) and cationic (methylene blue, MB) dyes removal from aqueous solutions. The swelling ratio of hydrogels prepared with 2 % CS and 2 % CMC (CS2/CMC2) exhibited optimal performance at different pHs. The addition of PEG into hydrogels (denoted as CS2/CMC2-PEG1.25) exhibited a significantly higher adsorption for CR and MB, increasing from 117.83 to 159.12 mg/g and 110.2 to 136 mg/g, respectively. The comprehensive analyses of Fourier transform infrared spectroscopy, thermalgravimetric study and scanning electron microscopy showed that CS2/CMC2-PEG1.25 hydrogels became more porous with no significant changes in intermolecular and intramolecular interactions, compared with CS2/CMC2 hydrogels. The adsorption process for CR and MB conformed to the pseudo-second-order and pseudo-first-order kinetics models, respectively. The results of adsorption isotherm for CR followed both Freundlich and Langmuir models with the maximum adsorption capacities of 1053.88 mg/g, whereas the isotherm for MB fitted the Langmuir model better with the maximum adsorption capacities of 331.72 mg/g. The thermodynamic study results proved that the CR and MB adsorption by hydrogels was spontaneous, but the CR adsorption was endothermic and the MB adsorption was exothermic.

Hesperidin partly ameliorates the decabromodiphenyl ether-induced reproductive toxicity in pubertal mice.

Many materials use polybrominated diphenyl ethers (PBDEs) as flame retardants. As one of the most common congeners of PBDEs, decabromodiphenyl ether (PBDE-209) is reported to harm reproductive health. However, little is known research on attenuating the reproductive toxicity induced by PBDE-209. The present study aimed to investigate the effects of hesperidin against PBDE-209-induced reproductive toxicity in male mice. Pubertal male C57BL/6 J mice were exposed to PBDE-209 groups (20, 100, 500 mg/kg·bw) and hesperidin groups (100 mg/kg·bw PBDE-209 + 100 mg/kg·bw hesperidin) for 8 weeks. The results showed that PBDE-209 increased the amount of abnormal morphological sperms and decreased the sex hormone levels. PBDE-209 induced the histopathological lesions of seminiferous tubules and blood-testis barrier in mice testis. Expressions of apoptosis-associated proteins and mRNA (Bax, Bcl-2, etc.) were altered by the PBDE-209 treatment. PBDE-209 prominently increased the malondialdehyde (MDA) levels, the biomarker of oxidative stress. Hesperidin treatment partly alleviated PBDE-209-induced histopathological lesions and apoptosis in mice testis. These findings suggested that hesperidin partly protects against PBDE-induced reproductive toxicity in pubertal mice. We conclude that more work needs to be done to explore the appropriate dosage of hesperidin or find other drugs to protect against the reproductive toxicity of PBDEs.

Chitosan-based oral colon-specific delivery systems for polyphenols: recent advances and emerging trends.

Oral colon-targeted delivery systems (OCDSs) have attracted great attention in the delivery of active compounds targeted to the colon for the treatment of colon and non-colon diseases with the advantages of enhanced efficacy and reduced side effects. Chitosan, the second-most abundant biopolymer next to cellulose, has great biocompatibility, is non-toxic, is sensitive to colonic flora and shows strong adhesion to colonic mucus, making it an ideal biomaterial candidate for the construction of OCDSs. Being rich in functional groups, the chitosan structure is easily modified, both physically and chemically, for the fabrication of delivery systems with diverse geometries, including nanoparticles, microspheres/microparticles, and hydrogels, that are resistant to the harsh environment of the upper gastrointestinal tract (GIT). This review offers a detailed overview of the preparation of chitosan-based delivery systems as the basis for building OCDSs. A variety of natural polyphenols with potent biological activities are used to treat diseases of the colon, or to be metabolized as active ingredients by colonic microorganisms to intervene in remote organ diseases after absorption into the circulation. However, the poor solubility of polyphenols limits their application, and the acidic environment of the upper GIT and various enzymes in the small intestine disrupt their structure and activity. As a result, the development of OCDSs for polyphenols has become an emerging and popular area of current research in the past decade. Thus, the second objective of this review is to systematically summarize the most recent research findings in this area and shed light on the future development of chitosan-based OCDSs for nutritional and biomedical applications.

High-fat diet exacerbated decabromodiphenyl ether-induced hepatocyte apoptosis via intensifying the transfer of Ca2+ from endoplasmic reticulum to mitochondria.

Polybrominated diphenyl ether (PBDE) as the flame retardant is heavily used in daily necessities, causing adverse health effects on humans. This study aimed to evaluate the hepatotoxicity of decabromodiphenyl ether (BDE-209), the most widely used PBDE, in lean and high-fat diet (HFD)-treated obese mice and elucidate the underlying mechanism. Firstly, the increasing levels of TG and proinflammatory factors in the liver and ALT and AST in serum demonstrated the hepatic damage caused by BDE-209 and further exacerbated by HFD. Tunel image revealed that BDE-209 induced more severe hepatocyte apoptosis with the assistant of HFD. Next, the mechanism analysis showed that the pro-apoptotic action of BDE-209 was in an endoplasmic reticulum (ER)/Ca2+ flux/mitochondria-dependent manner, concluded from the impairment of mitochondrial membrane potential, the enhancive protein expression of p-PERK/PERK, p-IRE1/IRE1, ATF6, CHOP, Bax/Bcl-2, cleaved caspase-3/caspase-3, IP3R1 and Sig-1R, and the over-transfer of Ca2+ from ER to mitochondria. Such proposed mechanism was further confirmed by the IP3R1 siRNA transfection cell experiment, where apoptotic rate was reduced in parallel with the reduced mitochondrial Ca2+ level. Finally, the higher expression of PACS-2 protein and the expanded ER contributed to the enriched ER-mitochondria interaction, reflected by the closer distance between ER and mitochondria visually displayed in the TEM image in HFD groups. This change was conducive to the rapid delivery of apoptosis signals via Ca2+, as proven, mechanically explaining the strengthening effect of HFD on BDE-209 hepatotoxicity. These findings detailedly explained the mechanism of BDE-209 hepatotoxicity and clarified the auxiliary effect of HFD, providing a theoretical basis for further studying other analogs.

Decabromodiphenyl ether initiates mitochondria-dependent apoptosis by disrupting calcium homeostasis in mice livers.

Decabromodiphenyl ether (BDE-209) tends to accumulate in lipid-rich tissues and targets the liver since its high lipophilicity. This study aimed to investigate the effects of BDE-209 on mouse liver and reveal the underlying toxicological mechanisms. Here we firstly confirmed that treatment of BDE-209 could lead to an imbalance of redox and promote apoptosis with a mitochondria-dependent manner in mice livers. Next, the transmission electron microscope (TEM) image revealed BDE-209 induced changes in mitochondrial morphology and increased endoplasmic reticulum (ER) - mitochondrial contact. ER stress was involved in the apoptosis process, which was displayed by the enhancive ER stress makers . Finally, from the increased abundance of cellular pivotal Ca2+ signals transducer CaM, activating Ca2+ release channel Sig-1R and IP3R1, and the stronger fluorescence density of mitochondria-specifically Ca2+ labeled probe Rhod-2 in vitro, we summarized that there was overloaded mitochondrial Ca2+ in hepatocytes of BDE-209 treated mice. In conclusion, these results partly illustrated evidence to reveal a potential mechanism of BDE-209-induced hepatoxicity, where oxidative stress-induced-ER stress led to the over-release of Ca2+, followed by the overloaded mitochondrial Ca2+, and cell apoptosis initiated. Our findings provided a theoretical basis for further studying.

The combined impact of decabromodiphenyl ether and high fat exposure on non-alcoholic fatty liver disease in vivo and in vitro.

Non-alcoholic fatty liver disease (NAFLD) is considered a public health concern. Decabromodiphenyl ether (BDE-209) and high fat (HF) exposure cause liver injury, yet the combined impact on NAFLD development remains unclear. HepG2 cells were incubated with BDE-209 or/and HF reagent (Csodium oleate/Csodium palmitate = 2/1) for establishing the in vitro model, while C57BL/6 mice fed BDE-209 or/and HF diet (HFD) was the in vivo model. Oil Red O staining and the determination of triglyceride, malondialdehyde, and reactive oxygen species (ROS) contents proved the elevated lipid accumulation and oxidative stress by the mixture of BDE-209 and HF in HepG2 cells, consistent in C57BL/6 mice. Importantly, the action analysis showed the synergistic effect between BDE-209 and HF, suggesting that the population preferring the HFD is more susceptible to BDE-209 to aggravate the progression of NAFLD. Further, the increased protein expression of sterol regulatory element-binding protein 1, fatty acid synthase, and stearoyl-CoA desaturase 1 was considered to be responsible for hepatic steatosis. The impairment of antioxidant system was reflected by the lower hepatic superoxide dismutase and glutathione transferase activities and reduced glutathione level, explaining the detected excessive ROS production. Besides, using high content analysis, the decline of mitochondrial mass and membrane potential, which was closed to the NAFLD pathogenesis, was also demonstrated in HepG2 cells.

Hesperidin prevents the combined toxicity of decabromodiphenyl ether and sodium nitrite in vitro.

Decabromodiphenyl ether (BDE-209) and Sodium nitrite (SN) coexist in the processing meat and fish foods, but there is no research considering them together. The present study aimed to investigate the binary mixture's toxicity of BDE-209 and SN and explore the protective effect of hesperidin (Hsp) on the combined toxicity. Results showed that compared with the impact of BDE-209 or SN alone, the binary mixture had a synergistic toxic effect on impairing the viability of HepG2 cells, accompanied by oxidative stress, Ca2+ accumulation, mitochondrial dysfunction. The increase of γ-H2AX fluorescent foci and micronuclei number also indicated its genotoxicity. Pretreatment of Hsp could significantly alleviate the above damage caused by the binary combination. These findings revealed the toxicological interaction of BDE-209 and SN and highlighted that food containing abundant natural flavonoids, as hesperidin, could reduce this toxicological risk.

Metabolic changes of Neurospora crassa in the presence of oleic acid for promoting lycopene production.

Neurospora crassa has been generally recognized as a safe organism and possesses a remarkable ability to produce yellow-to-orange carotenoids. The present work mainly explored the potential mechanism of exogenous oleic acid on promoting lycopene production in N. crassa. Carbon flux was conducively channelized into the mevalonate metabolic pathway to synthesize more lycopene, associating with the increased levels of acetyl-CoA, NADPH and factors related to the mevalonate pathway. Additionally, exogenous oleic acid boosted the intracellular triacylglycerol production through de novo and ex novo fatty acid synthesis pathways, which contributed to improving the accumulation of lycopene via lipid bodies. Further, the regulated fatty acid profile also enhanced the storage capacity of lipid bodies. Consequently, this study provided an effective strategy to enhance the lycopene production in N. crassa by adding oleic acid to the culture medium and elucidated an extraordinary insight into the potential mechanism.

Serum Cholesterol-Lowering Activity of ß-Sitosterol Laurate Is Attributed to the Reduction of Both Cholesterol Absorption and Bile Acids Reabsorption in Hamsters.

The research was performed to delineate how ß-sitosterol laurate (ß-SLE) consumption influenced serum and hepatic lipids. The results showed that 220 mg/5 mL oil/kg body weight of ß-SLE robustly reduced serum total triglyceride and cholesterol levels and the epididymal adipocyte size, and efficiently protected hepatic polyunsaturated fatty acids against lipid peroxidation through superoxide dismutase and glutathione transferase activity enhancement and malondialdehyde level reduction. Based on the changes of fecal cholesterol contents, fecal and hepatic bile acid (BAs) levels, and related protein expression, it was concluded that the mechanisms for lowering serum cholesterol by ß-SLE involved (i) the enhanced excretion of fecal cholesterol via down-regulation of intestinal Niemann-Pick C1-like 1 protein; (ii) the increased conversion from cholesterol to primary BAs via up-regulation of cholesterol-7α-hydroxylase and sterol 27-hydroxylase, which was induced by the reduced BAs reabsorption through up-regulating ileal apical sodium-dependent bile acid transporter and ileal bile acid-binding protein.

Consumption of Interesterified Medium- and Long-Chain Triacylglycerols Improves Lipid Metabolism and Reduces Inflammation in High-Fat Diet-Induced Obese Rats.

Medium- and long-chain triacylglycerols (MLCTs) were synthesized from rapeseed oil (RO), one kind of commonly used edible long-chain triacylglycerols (TGs), and then delivered to high-fat diet (HFD)-induced obese rats. Compared with RO, MLCT consumption exhibited more potent effects on reducing body and tissue weight gains, plasma TG, and total cholesterol (TC) levels and on improving hepatic TG, TC, fatty acid synthase, acetyl-CoA carboxylase, and lipoprteinlipase contents. Meanwhile, lower amounts of tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein-1, and endotoxin in plasma, lower levels of interleukin-6 and TNF-α, and higher levels of interleukin-10 in both livers and white adipose tissues were detected in MLCT-fed rats. MLCT intake also remarkably suppressed the size of adipocytes and the number of macrophages. In conclusion, our study suggested that the interesterified MLCT was more efficacious in improving the lipid metabolism and inflammation in HFD-induced obese rats than RO.

Changes in cell membrane properties and phospholipid fatty acids of bacillus subtilis induced by polyphenolic extract of Sanguisorba officinalis L.

Sanguisorba officinalis L. (family Rosaceae, subfamily Rosoideae) is a plant found throughout Southern Europe, Northern Africa, and Eastern Asia. This study demonstrated the antibacterial activity of a purified polyphenolic extract (PPE) from S. officinalis L. against Bacillus subtilis using growth inhibitory and apoptosis assays, and investigated the antibacterial mechanism responsible for changes in cell membrane properties. Fourier transform infrared spectroscopy suggested that PPE altered the cell wall and membrane properties of B. subtilis. Further determination of cell membrane integrity and permeability revealed that B. subtilis membrane integrity was more severely damaged by PPE at the minimum inhibitory concentration (MIC) than at the minimum bactericidal concentrati on (MBC). Instead, PPE at the MBC reduced cell membrane fluidity by significantly decreasing the proportion of anteiso- and iso-branched phospholipid fatty acids (PLFAs) from 64.17 ± 0.28% and 27.23 ± 0.03% in the control to 5.57 ± 1.06% and 6.00 ± 1.40%, respectively (P < 0.001). Scanning electron microscopy revealed different effects of PPE on cell morphology, demonstrating that, at the MIC and MBC, PPE exerted antibacterial activity by disrupting the cell membrane and reducing cell membrane fluidity, respectively. Consequently, this study elucidated changes in the bacterial membrane due to exposure to PPE and its potential use as an antimicrobial agent. PRACTICAL APPLICATION: The abuse of synthetic chemical preservatives raises food safety concerns; however, plant-derived polyphenolic compounds may be a safe and effective alternative. This study demonstrated the strong antibacterial activity of a purified polyphenolic extract (PPE) of Sanguisorba officinalis L. and revealed its antibacterial mechanism against Bacillus subtilis, suggesting that it may provide a useful antimicrobial agent in food industry applications.

Enzymatic Synthesis of ß-Sitosterol Laurate by Candida rugosa Lipase AY30 in the Water/AOT/Isooctane Reverse Micelle.

Phytosterols are regarded as compounds able to reduce total and low-density lipoprotein cholesterol in the blood, and their esterified derivatives could help to improve the effectiveness of this function. In the present study, the water/sodium 1,4-bis-2-ethylhexylsulfosuccinate (AOT)/isooctane reverse micelle (RM) system was set up as a reaction medium for Candida rugosa lipase AY30 (CRL AY30) to synthesize ß-sitosterol laurate (ß-SLE). The product was identified by TLC, FT-IR, and HPLC-APCI-QqQ-MS/MS and quantified by HPLC. Through stepwise optimization, it was found that CRL AY30 had the highest activity in the water/AOT/isooctane RM system where 50 mM PBS with a pH of 7.5 was adopted as water core to carry CRL AY30, and the proportion of [CRL AY30] (mg/mL), [water] (mM), and [AOT] (mM) was set in 3:375:25, respectively, in isooctane. After screened with single-factor experiments, the esterification reaction conditions in the CRL AY30-water/AOT/isooctane RM system were further optimized by the response surface method as follows: the mole ratio of ß-sitosterol to lauric acid of 1:3.5 (25 mM ß-sitosterol), the enzyme load of 18% (w/w total reactants), the reaction temperature of 47 °C, and the reaction time of 48 h. As a result, the maximum esterification rate was up to 88.12 ± 0.79%.