Alleviating sleep disturbances and modulating neuronal activity after ischemia: Evidence for the benefits of zolpidem in stroke recovery.

AIMS: Sleep disorders are prevalent among stroke survivors and impede stroke recovery, yet they are still insufficiently considered in the management of stroke patients, and the mechanisms by which they occur remain unclear. There is evidence that boosting phasic GABA signaling with zolpidem during the repair phase improves stroke recovery by enhancing neural plasticity; however, as a non-benzodiazepine hypnotic, the effects of zolpidem on post-stroke sleep disorders remain unclear. METHOD: Transient ischemic stroke in male rats was induced with a 30-minute middle cerebral artery occlusion. Zolpidem or vehicle was intraperitoneally delivered once daily from 2 to 7 days after the stroke, and the electroencephalogram and electromyogram were recorded simultaneously. At 24 h after ischemia, c-Fos immunostaining was used to assess the effect of transient ischemic stroke and acute zolpidem treatment on neuronal activity. RESULTS: In addition to the effects on reducing brain damage and mitigating behavioral deficits, repeated zolpidem treatment during the subacute phase of stroke quickly ameliorated circadian rhythm disruption, alleviated sleep fragmentation, and increased sleep depth in ischemic rats. Immunohistochemical staining showed that in contrast to robust activation in para-infarct and some remote areas by 24 h after the onset of focal ischemia, the activity of the ipsilateral suprachiasmatic nucleus, the biological rhythm center, was strongly suppressed. A single dose of zolpidem significantly upregulated c-Fos expression in the ipsilateral suprachiasmatic nucleus to levels comparable to the contralateral side. CONCLUSION: Stroke leads to suprachiasmatic nucleus dysfunction. Zolpidem restores suprachiasmatic nucleus activity and effectively alleviates post-stroke sleep disturbances, indicating its potential to promote stroke recovery.

Study on the treatment of corn alcohol wastewater by the internal circulation anaerobic reactor.

To comprehensively assess the efficacy of employing the internal circulation (IC) anaerobic reactor for corn alcohol wastewater treatment and investigate its feasibility, this study focused on anaerobic digestion parameters, energy balance, and the composition of the prokaryotic microbial community. During the operation of the reactor, the hydraulic retention time was progressively reduced from 4.8 to 1.6 days while achieving an average organic loading rate of 12.46 kg chemical oxygen demand (COD)/(m3·d). Moreover, the removal rate of COD exceeded 98%, and the energy balance (ΔE) reached 10.29 kJ/g fed COD. The initial manifestation of organic acidosis in the reactor was a decline in gas production, which is primarily caused by propionic acid accumulation. The subsequent analysis revealed a high diversity of prokaryotes in granular sludge, with the predominant archaea primarily involved in methane production through the acetic acid pathway. The IC anaerobic reactor shows exceptional performance in treating corn alcohol wastewater by optimizing its operating conditions. Energy balance analysis confirmed the feasibility of the process. The findings of this study may offer valuable insights for optimizing control strategies and engineering applications.

Melatonin supplementation in the subacute phase after ischemia alleviates postischemic sleep disturbances in rats.

BACKGROUND: Sleep disorders are highly prevalent among stroke survivors and impede stroke recovery. It is well established that melatonin has neuroprotective effects in animal models of ischemic stroke. However, as a modulator of endogenous physiological circadian rhythms, the effects of melatonin on poststroke sleep disorders remain unclear. In the present study, we investigated how melatonin delivered intraperitoneally once daily in the subacute phase after stroke onset, influencing neuronal survival, motor recovery, and sleep-wake profiles in rats. METHODS: Transient ischemic stroke in male Sprague-Dawley rats was induced with 30 min occlusion of the middle cerebral artery. Melatonin or vehicle was delivered intraperitoneally once daily in the subacute phase, from 2 to 7 days after stroke. Electroencephalogram and electromyogram recordings were obtained simultaneously. RESULTS: Compared to the effects observed in the vehicle-treated ischemic group, after 6 daily consecutive treatment of melatonin at 10 mg/kg starting at ischemic/reperfusion day 2, the infarct volume was significantly decreased (from 39.6 to 26.2%), and the degeneration of axons in the ipsilateral striatum and the contralateral corpus callosum were significantly alleviated. Sensorimotor performances were obviously improved as evidenced by significant increases in the latency to falling off the wire and in the use of the impaired forelimb. In addition to those predictable results of reducing brain tissue damage and mitigating behavioral deficits, repeated melatonin treatment during the subacute phase of stroke also alleviated sleep fragmentation through reducing sleep-wake stage transitions and stage bouts, together with increasing stage durations. Furthermore, daily administration of melatonin at 9 a.m. significantly increased the nonrapid eye movement sleep delta power during both the light and dark periods and decreased the degree of reduction of the circadian index. CONCLUSIONS: Melatonin promptly reversed ischemia-induced sleep disturbances. The neuroprotective effects of melatonin on ischemic injury may be partially associated with its role in sleep modulation.

Synergistic effect of chlorogenic acid and levofloxacin against Klebsiella pneumonia infection in vitro and in vivo.

The study aimed to investigate the antibacterial effect and potential mechanisms of chlorogenic acid (CA) in Klebsiella pneumonia (KPN) induced infection in vitro and in vivo. 62 KPN strains were collected from the First People's Hospital of Yunnan Province. CA and CA combined Levofloxacin (LFX) were detected for KPN biofilm (BF) formation in vitro. The lung infection mice model were established by KPN. The effect of CA (500 mg/kg), LFX (50 mg/kg) and CA combined LFX (250 mg/kg + 25 mg/kg) were evaluated through the survival of mice, the changes of inflammation factors of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1ß and IL-6 in serum, the histopathological analysis of lung and the protein expression of NLRP3 signaling pathway in vivo. A total of 62 KPNs were isolated and identified, of which 13 (21%) strains were BF positive. 8 (13%) strains were extended spectrum ß-lactamase strains (ESBLs), and 20 (32%) strains are ESBLs biofilm positive. In vitro study, CA and LFX showed a synergistic effect on KPN biofilm formation. In vivo mice experiment, CA, especially CA + LFX treated group significantly decreased the serum levels of TNF-α, IL-1ß and IL-6, improved the survival ratio and lung pathology changes, and also reduced the protein expression of ASC, caspase 1 p20, IL-1ß and phosphor NF-κB p65. CA could effectively alleviate lung infection of KPN infected mice, and the antibacterial effection is strengthened by combined with LFX. The study provide a theroy basis for making rational and scientific antibacterial therapy strategy in clinic.

Caffeine-stimulated muscle IL-6 mediates alleviation of non-alcoholic fatty liver disease.

Caffeine intake is associated with a reduced risk developing non-alcoholic fatty liver disease (NAFLD), but the underlying molecular mechanisms remain to be fully elucidated. We report here that caffeine markedly improved high fat diet-induced NAFLD in mice resulting in a 10-fold increase in circulating IL-6 levels, leading to STAT3 activation in the liver. Interestingly, the expression of IL-6 mRNA was not increased in the liver, but increased substantially in the muscles of caffeine-treated mice. Caffeine was found to stimulate IL-6 production in cultured myotubes but not in hepatocytes, adipocytes, or macrophages. The inhibition of p38/MAPK abrogated caffeine-induced IL-6 production in muscle cells. Caffeine failed to improve NAFLD in IL-6 and hepatocyte-specific STAT3 knockout mice, indicating that the IL-6/STAT3 pathway is vital for the hepatoprotective effects of caffeine in NAFLD. The possibility that IL-6/STAT3-mediated hepatic autophagosome induction and hepatocytic oxygen consumption are involved in the anti-NAFLD effects of caffeine cannot be excluded, based on the findings presented here. Our results reveal that caffeine ameliorates NAFLD via crosstalk between muscle IL-6 production and liver STAT3 activation.

Pu'erh tea extract-mediated protection against hepatosteatosis and insulin resistance in mice with diet-induced obesity is associated with the induction of de novo lipogenesis in visceral adipose tissue.

BACKGROUND: White adipose tissue (WAT) is important for the maintenance of metabolic homeostasis, and metabolic syndrome is sometimes associated with WAT dysfunction in humans and animals. WAT reportedly plays a key, beneficial role in the maintenance of glucose and lipid homeostasis during de novo lipogenesis (DNL). Pu'erh tea extract (PTE) can inhibit harmful, ectopic DNL in the liver, thus protecting against hepatosteatosis, in mice with diet-induced obesity. We examined whether PTE could induce DNL in WAT and consequently protect against hepatosteatosis. METHODS: C57BL/6 male mice were fed a high-fat diet (HFD) with/without PTE for 16 weeks. Systemic insulin sensitivity was determined using HOMA-IR, insulin- and glucose-tolerance tests, and WAT adipogenesis was evaluated by histological analysis. Adipogenesis-, inflammation-, and DNL-related gene expression in visceral AT (VAT) and subcutaneous AT (SAT) was measured using quantitative reverse transcription-PCR. Regression analysis was used to investigate the association between DNL in WAT and systemic insulin resistance or hepatosteatosis. RESULTS: Pu'erh tea extract significantly reduced the gain of body weight and SAT, but not VAT adiposity, in mice fed the high-fat diet and induced adipogenesis in VAT. The expression of DNL-related genes, including Glut4, encoding an important insulin-regulated glucose transporter (GLUT4), were highly elevated in VAT. Moreover, PTE inhibited VAT inflammation by simultaneously downregulating inflammatory molecules and inducing expression of Gpr120 that encodes an anti-inflammatory and pro-adipogenesis receptor (GPR-120) that recognizes unsaturated long-chain fatty acids, including DNL products. The expression of DNL-related genes in VAT was inversely correlated with hepatosteatosis and systemic insulin resistance. CONCLUSIONS: Activation of DNL in VAT may explain PTE-mediated alleviation of hepatosteatosis symptoms and systemic insulin resistance.

(-)-Epigallocatechin Gallate Targets Notch to Attenuate the Inflammatory Response in the Immediate Early Stage in Human Macrophages.

Inflammation plays important roles at different stages of diabetes mellitus, tumorigenesis, and cardiovascular diseases. (-)-Epigallocatechin gallate (EGCG) can attenuate inflammatory responses effectively. However, the immediate early mechanism of EGCG in inflammation remains unclear. Here, we showed that EGCG attenuated the inflammatory response in the immediate early stage of EGCG treatment by shutting off Notch signaling and that the effect did not involve the 67-kDa laminin receptor, the common receptor for EGCG. EGCG eliminated mature Notch from the cell membrane and the nuclear Notch intercellular domain, the active form of Notch, within 2 min by rapid degradation via the proteasome pathway. Transcription of the Notch target gene was downregulated simultaneously. Knockdown of Notch 1/2 expression by RNA interference impaired the downregulation of the inflammatory response elicited by EGCG. Further study showed that EGCG inhibited lipopolysaccharide-induced inflammation and turned off Notch signaling in human primary macrophages. Taken together, our results show that EGCG targets Notch to regulate the inflammatory response in the immediate early stage.

Pu-erh Tea Water Extract Mediates Cell Cycle Arrest and Apoptosis in MDA-MB-231 Human Breast Cancer Cells.

Pu-erh tea is believed to have health benefits, the growth inhibition activity of Pu-erh tea on breast cancer cell has not been investigated. In this study, we examined the activity of Pu-erh tea water extract on apoptosis and cell cycle arrest in the human breast adenocarcinoma cell line MDA-MB-231 and clarified its underlying mechanism of action. We found that Pu-erh tea extract inhibited cell proliferation and induced apoptosis in a dose-dependent manner. We also found that Pu-erh tea extract inhibited tumor cell growth within 24 h via accumulation of cells in S phase. Further experiments showed that at 24 h, Pu-erh tea extract up-regulated the expressions of P-p53 (Ser15), p21 and P-JNK and down-regulated the expressions of PCNA, CyclinD1 and CyclinE at the protein level in MDA-MB-231 cells. In particular, the JNK-specific inhibitor SP600125 restored the induction of P-JNK, P-p53 (Ser15), p21, CyclinD1 and CyclinE by Pu-erh tea extract. Our results indicate that Pu-erh tea water extract inhibits cell proliferation of MDA-MB-231 cells through the induction of apoptosis and the stimulation of cell cycle arrest, which is mediated via activation of the JNK-related pathway.

Oxidized tea polyphenols prevent lipid accumulation in liver and visceral white adipose tissue in rats.

BACKGROUND: Tea polyphenols are the prominent component in tea. After the fermentation process, tea polyphenols are oxidized by polyphenol oxidase to form oxidized tea polyphenols (OTPs). OTPs contain a significant amount of hydrophobic phenyl groups that can bind with non-aqueous materials. Here, we determined whether OTPs can bind with lipids and reduce fat uptake and assessed the effect of OTPs on decreasing obesity and alleviating hyperlipidaemia and other metabolic syndromes. METHODS: Rats were divided into three groups: control, high-fat diet (HFD) and OTP groups. The control and HFD groups were fed a chow diet and a high-fat diet, respectively, for 12 weeks; the OTP group was fed a high-fat diet for 6 weeks and then a high-fat diet containing 2 % OTP for 6 weeks. The serum and excrement triglyceride (TAG) and total cholesterol (CHOL) concentrations were determined, and liver tissue and white adipose tissue were collected to detect the expression levels of genes involved in lipid metabolism. RESULTS: Our results revealed that OTPs failed to decrease the serum concentrations of TAG and CHOL. OTPs alleviated the accumulation of lipids in the liver tissue and changed the expression levels of the regulators of lipid metabolism, i.e., peroxisome proliferation-activated receptors (ppars), compared with the rats fed a high-fat diet alone. We also observed a significantly decreased reduction of weight in the visceral white adipose, enhanced regulation of fatty acid ß-oxidation by PPARα and enhanced biosynthesis of mitochondria in the visceral white adipose of the OTP rats compared with the HFD rats. Additionally, OTPs promoted the excretion of lipids. CONCLUSION: Our results suggest that OTPs alleviate the accumulation of lipids in liver and visceral white adipose tissue and promote lipid excretion in rats in vivo.

Genome of Plant Maca (Lepidium meyenii) Illuminates Genomic Basis for High-Altitude Adaptation in the Central Andes.

Maca (Lepidium meyenii Walp, 2n = 8x = 64), belonging to the Brassicaceae family, is an economic plant cultivated in the central Andes sierra in Peru (4000-4500 m). Considering that the rapid uplift of the central Andes occurred 5-10 million years ago (Ma), an evolutionary question arises regarding how plants such as maca acquire high-altitude adaptation within a short geological period. Here, we report the high-quality genome assembly of maca, in which two closely spaced maca-specific whole-genome duplications (WGDs; ∼6.7 Ma) were identified. Comparative genomic analysis between maca and closely related Brassicaceae species revealed expansions of maca genes and gene families involved in abiotic stress response, hormone signaling pathway, and secondary metabolite biosynthesis via WGDs. The retention and subsequent functional divergence of many duplicated genes may account for the morphological and physiological changes (i.e., small leaf shape and self-fertility) in maca in a high-altitude environment. In addition, some duplicated maca genes were identified with functions in morphological adaptation (i.e., LEAF CURLING RESPONSIVENESS) and abiotic stress response (i.e., GLYCINE-RICH RNA-BINDING PROTEINS and DNA-DAMAGE-REPAIR/TOLERATION 2) under positive selection. Collectively, the maca genome provides useful information to understand the important roles of WGDs in the high-altitude adaptation of plants in the Andes.

Pu-erh tea extract ameliorates high-fat diet-induced nonalcoholic steatohepatitis and insulin resistance by modulating hepatic IL-6/STAT3 signaling in mice.

BACKGROUND: Pu-erh tea, made from the leaves of Camellia sinensis, possesses activities beneficial for human health, including anti-inflammatory, anti-oxidant, and anti-obesity properties. OBJECTIVE: We investigated the effects of a pu-erh tea extract (PTE) on nonalcoholic steatohepatitis (NASH) and the molecular mechanisms underlying such effects. METHODS: Eight-week-old male C57BL/6J mice were fed a normal chow diet or high-fat diet (HFD) for 17 weeks, during which PTE was simultaneously administered in drinking water. Body weight, hepatic inflammation, steatosis, insulin sensitivity, expression of lipogenesis- and gluconeogenesis-associated genes, and signal transducer and activator of transcription (STAT)-3 phosphorylation were examined. The anti-steatotic effects of PTE and/or interleukin (IL)-6 were evaluated in HepG2 cells. The lipid accumulation, STAT3 phosphorylation, and expression of lipid metabolism-related genes were analyzed. RESULTS: PTE inhibited HFD-induced obesity and significantly attenuated HFD-induced hepatic steatosis and liver inflammation, and prevented against liver injury. PTE treatment improved glucose tolerance and insulin sensitivity in HFD-fed mice. Moreover, PTE treatment maintained the intact insulin signal and significantly decreased expression of gluconeogenesis-related genes in the livers of HFD-fed mice. PTE treatment strikingly enhanced STAT3 phosphorylation in the livers of HFD-fed mice. Consistent with this increase in STAT3 phosphorylation, pre-treatment of HepG2 cells with PTE enhanced IL-6-induced STAT3 phosphorylation and attenuated oleic acid-induced steatosis in a STAT3-dependent manner. In contrast, PTE inhibited IL-6-induced STAT3 phosphorylation in macrophages. CONCLUSIONS: PTE ameliorates hepatic lipid metabolism, inflammation, and insulin resistance in mice with HFD-induced NASH, presumably by modulating hepatic IL-6/STAT3 signaling.

Caffeine is responsible for the bloodglucose-lowering effects of green tea and Puer tea extractsin BALB/c mice.

The present study was designed to determine the effects of Puer tea and green tea on blood glucose level. Male BALB/c mice were administered green tea extract (GTE) or Puer tea extract (PTE), either intragastrically or in their drinking water. The major components of these teas are epigallocatechin gallate (EGCG) and caffeine, respectively. Blood glucose measurement results showed that mice fed intragastrically or mice that drank GTE, PTE or caffeine showed significantly lower blood glucose levels compared to the control group. However, EGCG exhibited no influence on the blood glucose levels. When caffeine was eliminated from the GTE and PTE, the effect on the blood glucose levels was abolished, but the effect was recovered when caffeine was re-introduced into the extracts. Evaluation of hematological and biochemical indices at the time of the greatest caffeine-induced decrease in blood glucose levels showed that the effect of caffeine was specific. Microarray analyses were performed in 3T3-L1 preadipocytes and mature adipocytes treated with 0.1 mg · mL(-1) caffeine to identify factors that might be involved in the mechanisms underlying these effects. The results showed that few genes were changed after caffeine treatment in adipocytes, and of them only phospholipid transfer protein (PLTP) may be ralated to blood glucose. In conclusion, this study indicates that caffeine may be the key constituent of tea that decreases blood glucose levels, and it may be used to treat type 2 diabetes.

High quality reference genome of drumstick tree (Moringa oleifera Lam.), a potential perennial crop.

The drumstick tree (Moringa oleifera Lam.) is a perennial crop that has gained popularity in certain developing countries for its high-nutrition content and adaptability to arid and semi-arid environments. Here we report a high-quality draft genome sequence of M. oleifera. This assembly represents 91.78% of the estimated genome size and contains 19,465 protein-coding genes. Comparative genomic analysis between M. oleifera and related woody plant genomes helps clarify the general evolution of this species, while the identification of several species-specific gene families and positively selected genes in M. oleifera may help identify genes related to M. oleifera's high protein content, fast-growth, heat and stress tolerance. This reference genome greatly extends the basic research on M. oleifera, and may further promote applying genomics to enhanced breeding and improvement of M. oleifera.

The Genome of Dendrobium officinale Illuminates the Biology of the Important Traditional Chinese Orchid Herb.

Dendrobium officinale Kimura et Migo is a traditional Chinese orchid herb that has both ornamental value and a broad range of therapeutic effects. Here, we report the first de novo assembled 1.35 Gb genome sequences for D. officinale by combining the second-generation Illumina Hiseq 2000 and third-generation PacBio sequencing technologies. We found that orchids have a complete inflorescence gene set and have some specific inflorescence genes. We observed gene expansion in gene families related to fungus symbiosis and drought resistance. We analyzed biosynthesis pathways of medicinal components of D. officinale and found extensive duplication of SPS and SuSy genes, which are related to polysaccharide generation, and that the pathway of D. officinale alkaloid synthesis could be extended to generate 16-epivellosimine. The D. officinale genome assembly demonstrates a new approach to deciphering large complex genomes and, as an important orchid species and a traditional Chinese medicine, the D. officinale genome will facilitate future research on the evolution of orchid plants, as well as the study of medicinal components and potential genetic breeding of the dendrobe.

Oxaliplatin triggers necrosis as well as apoptosis in gastric cancer SGC-7901 cells.

Intrinsic apoptotic pathway is considered to be responsible for cell death induced by platinum anticancer drugs. While in this study, we found that, necrosis is an indispensable pathway besides apoptosis in oxaliplatin-treated gastric cancer SGC-7901 cells. Upon exposure to oxaliplatin, both apoptotic and necrotic features were observed. The majority of dead cells were double positive for Annexin V and propidium iodide (PI). Moreover, mitochondrial membrane potential collapsed and caspase cascades were activated. However, ultrastructural changes under transmission electron microscope, coupled with the release of cellular contents, demonstrated the rupture of the plasma membrane. Oxaliplatin administration did not stimulate reactive oxygen species (ROS) production and autophagy, but elevated the protein level of Bmf. In addition, receptor interacting protein 1 (RIP1), but not receptor interacting protein 3 (RIP3) and its downstream components participated in this death process. Necrostatin-1 (Nec-1) blocked oxaliplatin-induced cell death nearly completely, whereas z-VAD-fmk could partially suppress cell death. Oxaliplatin treatment resulted in poly(ADP-ribose) polymerase-1 (PARP-1) overactivation, as indicated by the increase of poly(ADP-ribose) (PAR), which led to NAD(+) and ATP depletion. PARP-1 inhibitor, olaparib, could significantly block oxaliplatin-induced cell death, thus confirming that PARP-1 activation is mainly responsible for the cytotoxicity of oxaliplatin. Phosphorylation of H2AX at Ser139 and translocalization of apoptosis-inducing factor (AIF) are critical for this death process. Taken together, these results indicate that oxaliplatin can bypass canonical cell death pathways to kill gastric cancer cells, which may be of therapeutic advantage in the treatment of gastric cancer.

Absorption of caffeine in fermented Pu-er tea is inhibited in mice.

Caffeine is present in a number of dietary sources consumed worldwide. Although its pharmacokinetics has been intensively explored, little is known about complexed caffeine (C-CAF) in aqueous extraction of fermented Pu-er tea. The major components of C-CAF are oxidative tea polyphenols (OTP) and caffeine. Furthermore, the C-CAF can be precipitated in low pH solution. After administering the same amount of total caffeine and comparing the peak level of plasma caffeine with the coffee (contains 0.11 ± 0.01% C-CAF) group, the results showed that the caffeine/OTP (contains 66.67 ± 0.02% C-CAF) group and the instant Pu-er tea (contains 23.18 ± 0.02% C-CAF) group were 33.39% and 25.86% lower, respectively. The concentration of the metabolites of caffeine supports the idea that the absorption of the C-CAF was inhibited in mice. Congruent with this result, the amount of caffeine detected in mice excrement showed that more caffeine was eliminated in the caffeine/OTP group and the Pu-er tea group. The locomotor activity tests of mice demonstrated that the stimulating effect of caffeine in caffeine/OTP and Pu-er tea was weaker than in coffee. Our findings demonstrate that caffeine can be combined with OTP and the absorption of C-CAF is inhibited in mice, thus decreasing the irritation effect of caffeine. This may also be developed as a slow release formulation of caffeine.

[Cloning and expression of single-chain Fv antibodies against H5N1 Avian influenza virus hemagglutinin].

To construct Fv antibodies against H5N1 Avian influenza virus hemagglutinin,extracted mRNA from B lymphoblastoid cell lines secreting anti-HA antibodies was used and the VH and VL genes were amplified by RT-PCR and linked together by splicing overlap extension (SOE) with (Gly4 Ser)3 linker. The recombinant plasmid was then transformed to E. coli BL21(DE3) and sequence analysis indicated the total length of scFv was 714 bp and the expression of Fv was validated by PAGE and Western blot.

[The triplet properties of beta-carotene in acetonitrile solution: a laser flash photolysis study].

The representative of carotenoids, beta-carotene, can scavenge reactive oxygen radicals like singlet molecular oxygen, nitrogen dioxide radical and peroxyl radical due to the effective antioxidative properties. In medicine, beta-carotene is used to alleviate the disease erythropoietic protoporphyria (EPP), by intercepting the triplet state of protoporphyrin (a porphyrin lacking a central metalion, a precursor to haem) therefore preventing the formation of singlet oxygen. Epidemiological evidence has suggested that dietary beta-carotene may inhibit certain types of cancer. Much of work has been carried out in benzene, toluene, or chloroform as most caroienoids are sufficiently soluble in these nonpolarity solvents. In the present paper, the generation and properties of triplet beta-carotene in acetonitrile solution were investigated with 355 nm laser flash photolysis. 2-acetonaphthone was used as an excitation energy donor to sensitize the production of the triplet state of beta-arotene. Excitation of the solution containing 2-acetonaphthone and beta-carotene upon 355 nm laser flash produced the triplet of 2-acetonaphthone (420 nm) firstly. Subsequently, the excitation energy of triplet 2-acetonaphthone was transferred to beta-carotene generating triplet beta-arotene. Characteristic absorption spectra of triplet beta-arotene (510 nm) were recorded. By means of transfer of excitation energy, the molar absorption coefficients of triplet beta-arotene were determined to be 23 000 dm3 mol(-1) x cm(-1) at 510 nm. The triplet lifetime for beta-carotene in acetonitrile solution was observed to be 15.6 micros. The rate constant for the reaction of triplet energy transfer from triplet 2-acetonaphthone to beta-carotene was calculated to be 1.5 x 10(10) dm3 x mol(-1) x s(-1). Obviously, the triplet beta-carotene has very low excitation energy. Taking the advantage of the photochemical properties of triplet beta-carotene, beta-Carotene has been widely used as energy acceptor to determine the excited state characteristic of other substance. This work extends the understanding of photochemical properties of beta-carotene.

Photoreactions of 1,4-naphthoquinone with lysozyme studied by laser flash photolysis and steady-state analysis.

Photoprocesses of 1,4-naphthoquinone (NQ) and its photoreactions with lysozyme in acetonitrile/water (3:1, v/v) solution were studied using 355 nm laser flash photolysis technique combined with electrophoresis and turbidimetric assay. The transient spectra of NQ were observed and the transient species were assigned. The electron transfer process from N,N,N',N'-tetramethyl-p-phenylenediamine (TMPD) to NQ triplet state ((3)NQ) was investigated and the rate constant was determined to be k(t1)=2.0 x 10(10)M(-1)s(-1). It has been found that (3)NQ can abstract hydrogen atom from lysozyme with a rate constant of k(t2)=2.4 x10(10)M(-1)s(-1). Furthermore, the results of steady-state analysis suggested that lysozyme can be damaged by NQ irradiated with UVA light influenced by the concentration of NQ and the gas saturated in the solution. The mechanisms of photosensitized damage of lysozyme were discussed.

Double roles of hydroxycinnamic acid derivatives in protection against lysozyme oxidation.

Oxidative damage to protein has been implicated in a number of diseases. Much interest has been focused on preventing oxidative damage to protein. Here we showed that hydroxycinnamic acid derivatives (HCA) were able to inhibit the cross-linking of protein induced by riboflavin-mediated photooxidation. HCA were also found to strongly protect lysozyme from gamma rays irradiation. The antioxidative properties of HCA were further studied by laser flash photolysis. Mechanism of antioxidant activities of HCA on lysozyme oxidation was discussed. HCA were found to protect protein against oxidation by scavenging oxidizing species and repairing the damaged protein.