Phytochemical characterization and radical scavenger activity of flavonoids from Helichrysum italicum G. Don (Compositae)

The glycosidic fraction of the flavonoids extracted from the flowering tops of the Helichrysum italicum G. Don was isolated, purified and characterized. This fraction was constituted by three compounds, which were assigned the structure of 4,2',4',6'-tetrahydroxychalcone-2'-glucoside, kaempferol-3-glucoside and naringenin-glycoside. Radical scavenger properties of the single glycosyl-flavonoids and of the in toto glycosidic fraction were tested with in vitro systems where different reactive oxygen species are generated (superoxide ions, hydroxyl radicals) and on lipid peroxidation induced by ADP/Fe2+ and NADPH or CCl4 in rat liver microsomes. The formation of reactive oxygen species was detected by cytochrome c reduction, salicylic acid hydroxylation and hyaluronic acid depolymerization. The action of the glycosidic fraction on the release of TXB2 and 12-HETE in human platelets, after collagen stimulation, was also evaluated. The glycosidic fraction inhibited in a dose dependent fashion lipid peroxidation in rat liver microsomes treated with ADP/Fe2+ or CCl4. This effect is due to the ability of flavonoids to scavenge free radicals at different stages of the process (superoxide ions, hydroxyl and lipid peroxide radicals). The single glycosyl-flavonoids exhibited a different scavenger activity, depending on the oxygen species and the chemical structure of the compounds. No effect of the fraction was observed on TXB2 and 12-HETE formation at 100 microns concentration.     

In vitro and in vivo antioxidant properties of different fractions of Moringa oleifera leaves

The antioxidant potency of different fractions of Moringa oleifera leaves were investigated by employing various established in vitro systems, such as β-Carotene bleaching, reducing power, DPPH/superoxide/hydroxyl radical scavenging, ferrous ion chelation and lipid peroxidation. On the basis of in vitro antioxidant properties polyphenolic fraction of M. oleifera leaves (MOEF) was chosen as the potent fraction and used for the DNA nicking and in vivo antioxidant properties. MOEF shows concentration dependent protection of oxidative DNA damage induced by HO and also found to inhibit the toxicity produced by CCl₄ administration as seen from the decreased lipid peroxides (LPO) and increased glutathione (GSH) levels. Among the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) levels were restored to almost normal levels compared to CCl₄ intoxicated rats. The HPLC analysis indicated the presence of phenolic acids (gallic, chlorogenic, ellagic and ferulic acid) and flavonoids (kaempferol, quercetin and rutin). Thus, it may be concluded that the MOEF possess high phenolic content and potent antioxidant properties, which may be mediated through direct trapping of the free radicals and also through metal chelation.     

Influence of oxygen on the inhibition of liver microsomal activation of carbon tetrachloride by the catechol 2-hydroxyestradiol-17β

In NADPH-supplied rat liver microsomes irreversible protein and lipid binding of ¹⁴C-CCl₄-metabolites continuously increase with decreasing oxygen concentrations. In aerobic suspensions of rat liver microsomes and NADPH the catechol steroid 2-hydroxyestradiol-17β effectively inhibits not only CCl₄-initiated lipid peroxidation but also protein and lipid binding of ¹⁴C-CCl₄-metabolites. With decreasing oxygen concentrations the inhibitory potency of 2-hydroxyestradiol-17β on all three parameters connected with activation of CCl₄ is reduced. In order to obtain the same inhibitory effect more catechol compound is needed under low than under high oxygen tensions. Anaerobically, 2-hydroxyestradiol-17β was found not to inhibit irreversible protein and lipid binding and lipid peroxidation was not detectable in absence of oxygen. An oxidized catechol metabolite rather than the catechol molecule itself may be responsible for the enzymatic inhibition of the activation step of CCl₄ or may interfere with reactions of the CCl₃-radicals formed.     

AMELIORIATION OF CHEMICALLY-INDUCED HEPATOCYTE INJURY BY CYCLOSPORINE A

Cyclosporine A, beside its current applications, possesses potential hepatoprotective effects. This study was directed to investigate the effect of Cyclosporine A pretreatment on hepatic injury due to carbon tetrachloride (CCl₄) and -galactosamine. Rats were injected by two successive doses of Cyclosporine A (5mgkg⁻¹day⁻¹). Six hours after the second dose, 1mlkg⁻¹of CCl₄was administered i.p. Effects associated with Cyclosporine A pretreatment were examined by using isolated hepatocytes and hepatocytes that were immobilized and continuously perfused. -Galactosamine (5m ) was added directly to the perfusion medium. After isolation, hepatocytes were examined histologically by light and electron microscopy, immobilized and perfused for further metabolic functional activity evaluation. Cyclosporine A pretreatmentin vivoproduced hepatoameliorative effects of various degrees which were statistically significant as manifested by: (1) an increased trypan blue exclusion after CCl₄; (2) an improved ureagenesis after CCl₄; (3) a reduction in the lipid droplets accumulation in the cytoplasm produced by CCl₄administration; (4) well preserved cytoplasmic organelles as mitochondria, endoplasmic reticulum ER, nuclear chromatin structures that were altered by CCl₄; and (5) an increased hepatocytes survival in the agarose gel matrix, reduction of LD leakage and improvement of ureagenesis after -galactosamine addition to the perfusion medium. The beneficial effect of Cyclosporine A pretreatment in modifying hepatotoxicity of chemical insults merits further studies.     

Free radical scavenging and antiatherogenic activities of Sesamum indicum seed extracts in chemical and biological model systems

An emerging consensus underscores the importance of oxidative events in vascular disease including excess production of reactive oxygen/nitrogen species (ROS/RNS), in addition to lipoprotein oxidation. Sesamum indicum has long been used extensively as a traditional food. The aim of present study was to evaluate antioxidant action of aqueous and ethanolic seed extracts from S. indicum using various in vitro ROS/RNS generated chemical and biological models. Results demonstrated that the graded-dose (25–1000 μg/ml) of aqueous and ethanolic extracts markedly scavenged the nitric oxide, superoxide, hydroxyl, 1,1-diphenyl-2-picrylhydrazyl and 2,2′-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid) radicals and, showed metal chelating ability as well as reducing capacity in Fe³⁺/ferricyanide complex and ferric reducing antioxidant power assays. In biological models, both extracts were found to inhibit metal-induced lipid peroxidation in mitochondrial fractions, human serum and LDL oxidation models. In lipoprotein kinetics study, both extracts significantly (P < 0.05) increased lag phase time along with reduced oxidation rate and conjugated dienes production. Ethanolic extract of S. indicum showed higher amounts of total polyphenol and flavonoid content as compared to their counterpart. The IC₅₀ values of both extracts were compared with respective antioxidant standards. Overall, ethanolic extract of S. indicum possess strong antioxidant capacity and offering effective protection against LDL oxidation susceptibility.     

Carbon tetrachloride-induced changes in adrenal microsomal mixed-function oxidases and lipid peroxidation

Studies were carried out to compare the effects of carbon tetrachloride (CCl₄) in vivo and in vitro on adrenal and hepatic microsomal metabolism in guinea pigs. CCl₄ administration in vivo decreased adrenal and hepatic microsomal cytochrome P-450 concentrations and lowered benzphetamine (BZ) demethylase and benzo[a]pyrene (BP) hydroxylase activities in both tissues. NADPH-cytochrome c reductase activity was decreased in hepatic but not in adrenal microsomes. Addition of CCl₄ to adrenal or hepatic microsomes in vitro produced a type I difference spectrum suggesting binding of CCl₄ to cytochrome(s) P-450; its magnitude was far greater in adrenal than in liver. Incubation of adrenal or hepatic microsomes in vitro with CCl₄ alone had little or no effect on mixed-function oxidase activity or on lipid peroxidation. However, when microsomes were incubated with CCl₄ + NADPH, the rates of BZ and BP metabolism were decreased, cytochrome P-450 concentrations were decreased, and lipid peroxidation was increased. The effects of CCl₄ + NADPH on enzyme activities were greater in adrenal than in hepatic microsomes. Addition of 1.0 mM EDTA or 0.1 mM MnCl₂ to the incubation medium blocked the effects of CCl₄ + NADPH on lipid peroxidation in adrenal and liver but had no effect on the decreases in mixed-function oxidase activities. The results indicate the following: (1) the adrenal cortex in the guinea pig is an active site of CCl₄ metabolism; (2) CCl₄ metabolism results in a loss of microsomal enzyme activities in the adrenal as well as liver; and (3) lipid peroxidation is not obligatory for the CCl₄-mediated destruction of microsomal enzymes.     

Nonionic surfactants are strong inhibitors of cytochrome P450 3A biotransformation activity in vitro and in vivo

Nonionic surfactants are commonly used as excipients in pharmaceutical formulation, but recent studies demonstrate that the ingredients affect the pharmacokinetics of the active drugs. However, the mechanisms are largely unknown. Here, we examined the effects of four common nonionic surfactants polysorbate 20, polyoxyl 35 castor oil, polyoxyl 40 stearate and poloxamer 188, on cytochrome P450 3A in vitro and in vivo using midazolam as a probe. We first examined the effects of these surfactants on the 1′-hydroxylation of midazolam in isolated rat liver and intestinal microsomes. All the surfactants tested inhibited midazolam 1′-hydroxylation in a concentration-dependent manner and presented a mixed competitive inhibitory model with decreased V_max and increased K_m values in vitro. Among the tested nonionic surfactants, polysorbate 20 was the most potent inhibitor of midazolam 1′-hydroxylation with an IC₅₀ of 2.06 and 0.39 mg ml⁻¹ in the liver and intestinal microsomes, respectively. These surfactants were also tested in vivo as we investigated their effects on the pharmacokinetics of midazolam in rats. These four surfactants displayed different inhibitory patterns in terms of the AUC of midazolam and 1′-hydroxymidazolam. Polysorbate 20 significantly increased both AUC_0–4 h and AUC_0–∞ of midazolam and decreased the AUC_0–4 h of 1′-hydroxymidazolam to about 40% (p < 0.05) in both single- and multiple-treated rats, along with a significant decrease of the metabolic ratio of 1′-hydroxymidazolam/midazolam to 25%. Polyoxyl 35 castor oil, polyoxyl 40 stearate and poloxamer 188 displayed complicated inhibition on the 1′-hydroxylation of midazolam dependent on the administration formula. These results confirmed that effects of these surfactants would have potential inhibitory effects on cytochrome P450 3A and altered midazolam bioavailability. Therefore, caution is needed when selecting nonionic surfactants in drug formulation.     

Inhibitory effect of Lysichiton camtschatcense extracts on Fe2+/ascorbate-induced lipid peroxidation in rat kidney and brain homogenates

Lysichiton camtschatcense is a well-known plant in Japan where it has been used as a traditional medicine by the “Ainu” people for the treatment of acute nephritis. It is presumed that L. camtschatcense has an inhibitory effect against nephritis caused by reactive oxygen species (ROS) owing to its antioxidant activities. Consequently, the antioxidant effect of L. camtschatcense extracts was assessed against Fe²⁺/ascorbic acid (AsA)-induced lipid peroxidation in rat kidney and brain homogenates. The antioxidant effect of the chloroform extract (CE) was more potent than that of the methanol extract (ME) for both homogenates. The antioxidant effect of both extracts was similar to those of α-tocopherol, a lipid-soluble antioxidant, and glutathione (GSH), a water-soluble antioxidant, which were used as reference compounds. Although CE showed a low radical-scavenging effect for superoxide anion radicals (O₂^·−) and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals, assessed by using an electron spin resonance (ESR) method, hydroxyl radicals (·OH) were markedly scavenged by more than 80%. On the other hand, ME showed more significant scavenging effect for DPPH radicals and O₂^·− than CE. These results suggest that the inhibitory effects of the L. camtschatcense extract on lipid peroxidation in rat kidney and brain are based on its high radical-scavenging effect against ·OH, O₂^·−, and lipid-derived radicals generated from the cell membrane.     

Interaction of trichloromethyl radicals with phenylalanine

Chemically or enzymatically generated trichloromethyl free radicals interact with liposoluble derivatives of phenylalanine. In vitro, in a chemical system to produce ·CCl₃ (benzoyl peroxide catalysis), this radical attacked N-acetyl-d,l-phenylalanine methyl ester (PheMeAc) to give a monochlorinated derivative (I) and an unsaturated imine type derivative of PheMeAc (II). Using a liver microsomal system to produce ·CCl₃ (microsomes + NADPH + CCl₄ under nitrogen), the attack of PheMeAc did not result in I or II formation, but in production of benzene. The phenylalanine content in liver microsomal proteins from rats treated with CCl₄ 6 h before, was not significantly decreased. The results suggest that phenylalanine is a potential target of ·CCl₃.This work was partially supported by a Grant from the National Institutes of Health (USA)     

Effects of Nonanal,trans-2-Nonenal and 4-Hydroxy-2,3-trans-nonenal on Cyclooxygenase and 12-Lipoxygenase Metabolism of Arachidonic Acid in Rabbit Platelets

The effects of nonanal, trans-2-nonenal and 4-hydroxy-2,3-trans-nonenal on the formation of thromboxane B₂ (TXB₂), 12-hydroxy-5,8,10-heptadecatrienoic acid (HHT) and 12-hydroxy-5,8,10,14-eicosatetraenoic acid (12-HETE) from exogenous arachidonic acid in washed rabbit platelets were examined. Nonanal and trans-2-nonenal at concentrations ranging from 0.25 to 2 μm inhibited TXB₂, HHT and 12-HETE formation, reducing the amounts of these three arachidonic acid metabolites by 50% at nonanal and trans-2-nonenal concentrations of approximately 0.25 μm. The inhibition of TXB₂, HHT and 12-HETE formation induced by 4-hydroxy-2,3-trans-nonenal (50% inhibition by 4-hydroxy-2,3-trans-nonenal at a concentration of approximately 100 μm) was 400 times weaker than that induced by nonanal and trans-2-nonenal. These results suggest that nonanal and trans-2-nonenal can be modulators of platelet arachidonic acid metabolism by affecting the activity of cyclooxygenase and 12-lipoxygenase.     

Altered Pharmacokinetics of Paclitaxel in Experimental Hepatic or Renal Failure

No HeadingPurpose. The aim of this study was to investigate the effect of hepatic or renal insufficiency on the pharmacokinetics of paclitaxel in rats.Methods. Rats were treated with carbon tetrachloride (CCl₄; 0.5 ml/kg) to induce hepatic failure or were subjected to 5/6 nephrectomy (5/6 Nx) to induce renal failure. Paclitaxel (3 mg/kg) was administered intravenously or intraportally. Testosterone 6-hydroxylase activity, which is a marker of CYP3A activity, was measured in rat liver microsomes from CCl₄-treated or 5/6 Nx rats.Results. After paclitaxel was administered intravenously, total body clearance was significantly reduced by 73% and 34% relative to each control value in CCl₄-treated and 5/6 Nx rats, respectively (control, 1.82 ± 0.42 vs. CCl₄-treated, 0.49 ± 0.11; sham, 1.54 ± 0.07 vs. 5/6 Nx, 1.01 ± 0.12 L h^–1 kg^–1; mean ± SE, n = 5 to 6). Testosterone 6-hydroxylase activity was reduced by 92% and 59% relative to each control value in rat liver microsomes from CCl₄-treated and 5/6 Nx rats, respectively. After the intraportal administration of paclitaxel, apparent clearance was reduced by 85% relative to control value in rats with hepatic failure, while that in rats with renal failure was the same as the reduction in systemic clearance.Conclusions. These results suggested that not only hepatic failure but also renal failure could modify the pharmacokinetics of paclitaxel in vivo.     

Irreversible binding of 14C from 14CCl4 to liver microsomal lipids and proteins from rats pretreated with compounds altering microsomal mixed-function oxygenase activity

¹⁴C from ¹⁴CCl₄ irreversibly binds to lipid and protein components of different liver subcellular fractions. Microsomal lipids bind more ¹⁴C than does either mitochondria or 105,000 g supernatant. The proteins from the 105,000 g fraction bind more ¹⁴C than those from the other two fractions. The extent of the irreversible binding of ¹⁴C to microsomal lipids and proteins is decreased by the prior treatment of the rats with cystamine, pyrazole, 3-methylcholanthrene or metopirone while it is increased by pretreatment with phenobarbital. The prior treatment with 2-diethylaminoethyl 2,2-diphenyl valerate hydrochloride (SKF 525A) increased the irreversible binding of ¹⁴C to microsomal lipids, but not to microsomal proteins. The results suggest that the irreversible binding of ¹⁴C to microsomal lipids is a more reliable expression of the CCl₄-activation step than the one to microsomal proteins. The ¹⁴CCl₃ free radicals responsible for the binding of ¹⁴C to lipid would arise during the reduction of the CCl₄/cytochrome P-450 complex mediated by cytochrome P-450 reductase.     

Potentiation by carbon tetrachloride of NADPH-dependent lipid peroxidation in lung microsomes.

NADPH-dependent lipid peroxidation occurs in rat lung microsomes in vitro. Expressed per wet weight of tissue we found that lung had only $\text{1}\text{100}$ the activity of liver. However, examination of the rate of malonyl dialdehyde production with different concentrations of NADPH revealed that the kinetics of lipid peroxidation in lung microsomes was indistinguishable from that of NADPH-dependent lipid peroxidation in liver microsomes. With lung microsomes supplemented with NADPH, lipid peroxidation was potentiated by CCl₄ and inhibited by EDTA, Mn²⁺, and cytochrome c.     

Cyanidin-3-glucoside Inhibits ATP-induced Intracellular Free Ca2+ Concentration,ROS Formation and Mitochondrial Depolarization in PC12 Cells

Flavonoids have an ability to suppress various ion channels. We determined whether one of flavonoids, cyanidin-3-glucoside, affects adenosine 5''-triphosphate (ATP)-induced calcium signaling using digital imaging methods for intracellular free Ca²⁺ concentration ([Ca²⁺]_i), reactive oxygen species (ROS) and mitochondrial membrane potential in PC12 cells. Treatment with ATP (100µM) for 90 sec induced [Ca²⁺]_i increases in PC12 cells. Pretreatment with cyanidin-3-glucoside (1µ g/ml to 100µg/ml) for 30 min inhibited the ATP-induced [Ca²⁺]_i increases in a concentration-dependent manner (IC₅₀=15.3µg/ml). Pretreatment with cyanidin-3-glucoside (15µg/ml) for 30 min significantly inhibited the ATP-induced [Ca²⁺]_i responses following removal of extracellular Ca²⁺ or depletion of intracellular [Ca²⁺]_i stores. Cyanidin-3-glucoside also significantly inhibited the relatively specific P2X2 receptor agonist 2-MeSATP-induced [Ca²⁺]_i responses. Cyanidin-3-glucoside significantly inhibited the thapsigargin or ATP-induced store-operated calcium entry. Cyanidin-3-glucoside significantly inhibited the ATP-induced [Ca²⁺]_i responses in the presence of nimodipine and ω-conotoxin. Cyanidin-3-glucoside also significantly inhibited KCl (50 mM)-induced [Ca²⁺]_i increases. Cyanidin-3-glucoside significantly inhibited ATP-induced mitochondrial depolarization. The intracellular Ca²⁺ chelator BAPTA-AM or the mitochondrial Ca²⁺ uniporter inhibitor RU360 blocked the ATP-induced mitochondrial depolarization in the presence of cyanidin-3-glucoside. Cyanidin-3-glucoside blocked ATP-induced formation of ROS. BAPTA-AM further decreased the formation of ROS in the presence of cyanidin-3-glucoside. All these results suggest that cyanidin-3-glucoside inhibits ATP-induced calcium signaling in PC12 cells by inhibiting multiple pathways which are the influx of extracellular Ca²⁺ through the nimodipine and ω-conotoxin-sensitive and -insensitive pathways and the release of Ca²⁺ from intracellular stores. In addition, cyanidin-3-glucoside inhibits ATP-induced formation of ROS by inhibiting Ca²⁺-induced mitochondrial depolarization.     

Hepatoprotective action of nine constituents isolated from the leaves of Clausena lansium in mice

The hepatoprotective actions of nine compounds isolated from the leaves of Clausena lansium (Loor.) Skeels, Rutaceae were studied. The nine compounds at the dose of 250 mg/kg, except demethylsecoclausenamide, significantly depressed the elevated serum transaminase in mice intoxicated with CCl₄. Further study on the more abundant components, seco-clausenamide and clausenamide, demonstrated that both compounds decreased the hepatotoxicity of thioacetamide and acetaminophen in mice. Clausenamide was shown to significantly inhibit CCl₄-induced lipid peroxidation of liver microsomes and ¹⁴C-CCl₄ covalent binding to microsomal lipids. The results indicate that eight compounds isolated from Clausena lansium have hepatoprotective activity in mice. Drug Dev. Res. 39:174–178. © 1997 Wiley-Liss, Inc.     

Destruction of liver microsomal calcium pump activity by carbon tetrachloride and bromotrichloromethane

Disturbed cellular calcium homeostatis has been observed during carbon tetrachloride (CCl₄) poisoning, with large alterations in calcium content occurring 8 hr after administration. Moore el at. [10] have shown that the hepatic smooth endoplasmic reticulum can sequester calcium and that this ability is decreased severely within 30 min after CCl₄ administration to rats. It was suggested that disturbed endoplasmic reticulum calcium pump activity may have a critical role in the expression of CCl₄ hepatotoxicity. We examined the effect of bromotrichloromethane (BrCCl₃) and CCl₄ metabolism on the calcium pump of Fe²⁺-free rat liver microsomes. It was determined that severe deficits in calcium uptake can be correlated with minimal lipid peroxidation induced by these agents. At a given level of lipid peroxidation, calcium uptake was affected more severely than were the activities of the microsomal enzymes glucose-6-phosphatase and aminopyrine demethylase. Calcium uptake was increased 7-fold by the presence of 5 mM ATP in incubations prior to assay of calcium sequestration. Lipid peroxidation induced by BrCCl₃-NADPH was accompanied by leakage of calcium from calcium-loaded microsomes. These results strengthen the possibility that disturbances in intracellular calcium homeostasis may be a key event in liver injury induced by BrCCl₃ and CCl₄.     

Adriamycin stimulates NADPH-dependent lipid peroxidation in liver microsomes not only by enhancing the production of O2∸ and H2O2, but also by potentiating the catalytic activity of ferrous ions

The antitumor drug, adriamycin, enhances NADPH-dependent lipid peroxidation in liver microsomes via the formation of Superoxide anion radicals (O₂^?) and hydrogen peroxide (H₂O₂). In the presence of metal ions additional reactive species are generated, causing stimulation of lipid peroxidation.However, in this study it was found that the stimulation of NADPH-dependent lipid peroxidation by adriamycin was not only affected by the production of O₂^? and H₂O₂. Adriamycin also enhances the catalysis by metal ions of the formation of those reactive oxygen species which initiate peroxidation. This was inferred from the fact that adriamycin stimulated malondialdehyde production at low ferrous ion concentrations, whereas at high ferrous ion concentrations no stimulation was found. Additional evidence was found in experiments in which the enzymic redox cycle of adriamycin in microsomes was abolished by heat-inactivation of the microsomes, and O₂^? and H₂O₂ were only produced with xanthine and xanthine oxidase. In this case in the presence of ferrous ions, adriamycin stimulated lipid peroxidation.     

Effects of Embelin on Lipid Peroxidation and Free Radical Scavenging Activity against Liver Damage in Rats

Abstract: The study aimed to evaluate the hepatic antioxidant capacity of embelin (from Embelia ribes) using different antioxidant tests, free radical scavenging activity and lipid peroxidation in albino rats. Carbon tetrachloride (CCl₄) treatment to rats has been more susceptible to peroxidative damage through production of reactive metabolites, namely trichloromethyl‐free radicals (CCl^?₃ and/or CCl₃OO^?) as measured by thiobarbituric acid reactive species. After the induction of liver damage by CCl₄ intoxication to rats, the concentration of lipid peroxidation was significantly (P ≤ 0.001) higher in liver and serum, along with concomitant decrease in the levels of antioxidants and cytochrome P450 enzyme in liver as compared to vehicle controls. The activities of marker enzymes – transaminases (AST, ALT), alkaline phosphatase (ALP), γ‐glutamyl transpeptidase (GGT), lactate dehydrogenase (LDH) – along with the total bilirubin and total protein levels were altered significantly (P ≤ 0.001) in the serum of CCl₄‐treated rats. When these rats received embelin orally (25 mg/kg) from day 1 to day 15, peroxidative damage was minimal in both liver and serum along with effectively inducing the antioxidant potential in CCl₄‐treated rats. The biochemical results were compared with the standard drug silymarin – a combination of flavonolignans of Silybum marianum and histology of liver sections. In conclusion, this study suggests that embelin acts as a natural antioxidant against hepatotoxicity induced in rats.     

藤梨根化学成分的研究

A number of constituents were isolated from the root of Actinidia chinensis Planch. Seven of them were indentified as physcion (emodin-6-methyl ether) (T₁), emodin (frangala-emodin) (T₂), emodin-8-β-D-glucoside (T₃), questin (emodin-8-methyl ether) (T₅), citreorosein (ω-hydroxyemodin) (T₆), emodic acid (T₇) and β-sitosterol (T₄).Comparison of the ¹HNMR data of emodin (T₂) and its 8-glucoside (T₃) shows that the aromatic proton experiences a downfield shift of about 0.5 ppm upon glycosidation of an ortho phenolic group, a fact which can be used to advantage for the allocation of the glycosidic linkage.     

Determination of free malonaldehyde formed in liver microsomes upon CCl4 oxidation

Free malonaldehyde formed in the microsomes prepared from livers of monkey, rat, rabbit, mouse, cow, pig, dog, sheep and horse upon CCl₄ oxidation was derivatized by reaction with N-methylhydrazine to form 1-methylpyrazole which was subsequently analyzed by capillary gas chromatography. Among the livers from animals tested, the monkey and rat livers produced the most malonaldehyde upon CCl₄ treatment. Horse liver showed the greatest resistance to CCl₄ oxidation. The gas chromatography method used in the present study exhibited an accurate and specific measurement of free malonaldehyde that might provide an understanding of the biochemical process of in vitro lipid peroxidation.