The effects of diazinon on lipid peroxidation and antioxidant enzymes in rat erythrocytes: role of vitamins E and C

Reactive oxygen species caused by organophosphates may be involved in the toxicity of various pesticides. Therefore, in this study, we aimed to investigate the effects of acute exposure to organophosphate insecticide diazinon (DI) and possible ameliorating role of vitamins E and C, with the following parameters: lipid peroxidation (LPO) and the activity of the glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) in rat erythrocytes. The experimental groups were arranged as control group, DI-treated group (DI) and DI + vitamin E + vitamin C-treated group (DI + Vit). DI + Vit groups were treated orally with a single dose of 335 mg/kg DI body weight. Vitamins E and C were injected at doses of 150 mg/kg body weight intramuscular (in) and 200 mg/kg body weight intraperitoneal (ip), respectively, 30 min after the treatment of DI in DI + Vit group. Blood samples were taken 24 h after the DI. The results showed that DI administration caused to increase in LPO and the activities of SOD and GSH-Px enzymes in erythrocytes. Also, the combination of vitamins E and C decreased LPO and the activities of GSH-Px and SOD compared with the DI group. In conclusion, although treating rats with single dose DI increases LPO and antioxidant enzyme activities in erythrocytes, vitamins C and E combination can reduce LPO caused by DI.     

Fallopian damage induced by organophosphate insecticide methyl parathion, and protective effect of vitamins E and C on ultrastructural changes in rats

The aim of the present study was to examine the effects of subchronic methyl parathion (MP) administration on lipid peroxidation and fallopian tube damage, and to evaluate the preventive effects of the use of vitamins E and C against toxicity. The experimental groups were: rats treated with corn oil (control group), with 5 mg/kg MP and with 5 mg/kg body weight MP plus vitamins E and C (MP + Vit). The groups were given MP by oral gavage for five days a week for four weeks at a daily dose of 5 mg/kg (MP and MP + Vit) using corn oil as a vehicle. Vitamins E and C were injected at doses of 50 mg/kg intramuscularly and 20 mg/kg intraperitoneally, respectively, just after the treatment with MP in the MP + Vit group. The levels of malondialdehyde (MDA) were determined in rat plasma. Electron microscopic ultrastuructural and histopathological changes in the fallopian tissue were examined. MDA levels were higher in the MP group than in the control group, and lower in the MP + Vit group than in the MP group. MP led to deletions in microvilli and marked loss in kinocillia of surface epithelium. But these marked histopathological findings decreased in the MP + Vit group. Multiple doses of MP administration caused some damage in the fallopian tube, and treatment with vitamins E and C after MP could reduce this effect.     

Energy-modulating vitamins--a new combinatorial therapy prevents cancer cachexia in rat mammary carcinoma

Mitochondria are the major intracellular organelles producing ATP molecules via the electron transport chain. Cancer cells have a deviant energy metabolism, and a high rate of glycolysis is related to a high degree of dedifferentiation and proliferation. The overall net ATP production is diminished with cancer, which ultimately leads to cancer cachexia. The present study was designed to investigate the altered energy metabolism in cancer cells and to enhance ATP production in the normal host cell metabolism by enhancing the activities of mitochondrial enzymes, using energy-modulating vitamins, and thus prevent cancer cachexia. Female Sprague-Dawley rats were selected for the experimental study. Mammary carcinoma was induced by the oral administration of 7,12-dimethylbenz[a]anthracene (25 mg/kg body weight), and treatment was started by the oral administration of the energy-modulating vitamins riboflavin (45 mg/kg body weight per d), niacin (100 mg/kg body weight per d) and coenzyme Q10 (40 mg/kg body weight per d) for 28 d. Mitochondria were isolated from the mammary gland and liver of all four groups, and the Krebs cycle and oxidative phosphorylation enzymes were assayed. In mammary carcinoma-bearing animals, the activities of the Krebs cycle and oxidative phosphorylation enzymes were significantly decreased. These activities were restored to a greater extent in animals treated with energy-modulating vitamins. From these experimental results, one may hypothesize that the combination therapy of energy-modulating vitamins could be of major therapeutic value in breast cancer.     

Hepatoprotective role of ferulic acid: a dose-dependent study

Alcohol use is contributing to an unprecedented decline in life expectancy. Damage to the liver after ethanol administration is a well-known phenomenon. Free radical mechanisms have been proposed to play a part in ethanol-induced liver toxicity. Ingestion of diets rich in polyunsaturated fatty acids (PUFAs) along with alcohol is known to result in enhanced liver damage. The present work is aimed at evaluating the protective role of ferulic acid, a naturally occurring plant component, on alcohol- and PUFA-induced liver toxicity. Three different doses of ferulic acid (10, 20, and 40 mg/kg of body weight) were administered to rats given alcohol, heated PUFA (DeltaPUFA), and alcohol + DeltaPUFA. Influence of ferulic acid on alcohol-and PUFA-induced liver damage was evaluated by analyzing the activities of the liver marker enzymes alkaline phosphatase, gamma-glutamyl transferase, alanine transaminase, and aspartate transaminase. The activities of these liver marker enzymes were increased in the alcohol, DeltaPUFA, and alcohol + DeltaPUFA groups but were decreased significantly on treatment with ferulic acid. The low dose (10 mg/kg of body weight) was not effective, but both 20 mg and 40 mg/kg of body weight were found to be effective. The 20 mg/kg of body weight dose was found to be more effective than 40 mg/kg of body weight (the high dose). The administration of ferulic acid to normal rats did not produce any harmful effects. Thus our results show that ferulic acid is an effective anti-hepatotoxic agent without side effects and may be a good candidate in the current search for a natural hepatoprotective agent.     

Effects of maternal administration of vitamins C and E on ethanol neurobehavioral teratogenicity in the guinea pig.

Consumption of ethanol during human pregnancy can produce a wide spectrum of teratogenic effects, including neurobehavioral dysfunction. This study, in the guinea pig, tested the hypothesis that chronic maternal administration of antioxidant vitamins C plus E, together with ethanol, mitigates ethanol neurobehavioral teratogenicity. Pregnant guinea pigs received one of the following four chronic oral regimens: ethanol and vitamins C plus E; ethanol and vitamin vehicle; isocaloric-sucrose/pair-feeding and vitamins C plus E; or isocaloric-sucrose/pair-feeding and vehicle. Vitamins C (250 mg) plus E (100mg) or vehicle were given daily, and ethanol (4 g/kg maternal body weight/day) (E) or isocaloric-sucrose/pair-feeding was given for 5 consecutive days followed by 2 days of no treatment each week throughout gestation. One neonate from selected litters was studied on postnatal day (PD) 0. Neurobehavioral function was determined by measuring task acquisition and task retention using an 8-day moving-platform version of the Morris water-maze task, starting on PD 45. Thereafter, in vivo electrophysiologic assessment of changes in hippocampal synaptic plasticity was conducted. There was an ethanol-induced decrease in neonatal brain weight compared with sucrose. The vitamins C plus E regimen protected hippocampal weight relative to brain weight in ethanol offspring, and mitigated the ethanol-induced deficit in the task-retention component of the water-maze task. However, in the sucrose group, this Vit regimen produced deficits in both task acquisition and task retention. The vitamins C plus E regimen did not mitigate the ethanol-induced impairment of hippocampal long-term potentiation. These results indicate that maternal administration of this high-dose vitamins C plus E regimen throughout gestation has limited efficacy and potential adverse effects as a therapeutic intervention for E neurobehavioral teratogenicity.     

Effect of supplementation of vitamin E and vitamin C on brain acetylcholinesterase activity and neurotransmitter levels in rats treated with scopolamine, an inducer of dementia

In the present study, the effects of vitamins E and C on the levels of neurotransmitters and acetylcholinesterase activity in the brains of rats treated with scopolamine, an inducer of dementia, were examined. Fifty male Sprague-Dawley rats at the age of 5 wk were divided into five groups after 1 wk of adaptation and fed five different diets for 6 wk: a no-scopolamine group, which was a scopolamine-untreated group fed only a basal diet: a scopolamine-treated group fed a basal diet; a vitamin E-supplemented scopolamine-treated group: a vitamin C-supplemented scopolamine-treated group; and a vitamins E and C-supplemented scopolamine-treated group. Scopolamine was twice administered by intraperitoneal injection (300 mg/kg, body weight), 3 d and 20 min prior to sacrifice. Brain acetylcholinesterase activity was markedly reduced by scopolamine injection. However, the supplementation of vitamins E and C in the diet significantly increased the reduced brain acetylcholinesterase activity up to the level of the scopolamine-untreated group. Brain serotonin concentration in the vitamin C-supplemented scopolamine-treated group was significantly higher than that in the scopolamine-treated group. However, there were no significant differences in brain dopamine and norepinephrine concentrations among all groups. In conclusion, supplementation with vitamin E and/or vitamin C might be useful in maintaining brain acetylcholinesterase activity at the normal level and serotonin concentration for some extent under the condition to induce dementia by scopolamine administration.     

The Aqueous Extract of Withania coagulans Fruit Partially Reverses Nicotinamide/Streptozotocin-Induced Diabetes Mellitus in Rats

Abstract Withania coagulans fruit has been shown to possess antihyperglycemic properties and is used in the traditional Indian system of medicine. However, there has no systematic study of its mechanism of action. In a rat model diabetes mellitus (DM) was induced by intraperitoneal injection of nicotinamide (230?mg/kg of body weight) followed by streptozotocin at 55?mg/kg of body weight. After 96?h, mildly diabetic (MD) (fasting plasma glucose [FPG]=7-11.1?mmol/L) and severely diabetic (SD) (FPG>11.1?mmol/L) rats were treated with aqueous extract of W. coagulans fruit at doses of 125, 250, and 500?mg/kg of body weight/day orally. FPG, postprandial plasma glucose (PPPG), glycosylated hemoglobin (HbA(1c)), plasma insulin, tissue glycogen, and glucose-metabolizing enzymes were assayed at Day 30. Treatment of diabetic animals (MD and SD) with different doses of aqueous W. coagulans resulted in significantly decreased FPG, PPPG, and HbA(1c) (P<.01), whereas serum insulin increased significantly compared with that in diabetic-untreated rats (P<.01). MD and SD animals treated with aqueous W. coagulans also showed significant increases in liver and muscle glycogen compared with diabetic-untreated animals (P<.01). Moreover, activities of glucokinase and phosphofructokinase were also significantly increased (P<.01), whereas glucose-6-phosphatase activity was significantly decreased (P<.01) in MD and SD groups treated with aqueous W. coagulans compared with diabetic-untreated groups. The most effective dose of aqueous W. coagulans was 250?mg/kg of body weight. These results show that the aqueous extract of W. coagulans fruit has significant antihyperglycemic effects, which may be through the modulation of insulin levels and related enzyme activities.     

Endotoxin and lipid peroxidation in vitro in selenium- and vitamin E-deficient and -adequate rat tissues

The effect of Salmonella typhimurium endotoxin injected intraperitoneally into rats (0.5 mg/kg of body weight) on subsequent lipid peroxidation in vitro was assessed. Peroxidation was monitored by measuring ethane production from tissue slices, as well as thiobarbituric acid-reactive substances and conjugated dienes in tissue homogenates. Weanling rats were fed a selenium- and vitamin E-deficient basal diet or one supplemented with 0.2 mg of Se/kg of diet and 200 mg of vitamin E/kg. After 9 to 16 wk, ethane production and thiobarbituric acid-reactive substances in liver and lung generally were increased by LPS treatment of Se- and vitamin E-deficient rats. Conjugated dienes were increased by LPS treatment in liver of Se- and vitamin E-deficient rats, but paradoxically, were higher in Se- and vitamin E-adequate liver tissue. Daily injections of 1 g of hydroxyurea/kg of body weight, a cell proliferation inhibitor, for 2 d prior to LPS injection significantly decreased the LPS-induced ethane production in Se- and vitamin E-deficient rat liver and lung. These results show that low doses of LPS injected into rats stimulated lipid peroxidation in vitro in Se- and vitamin E-deficient rat liver tissue. Hydroxyurea decreased LPS-induced lipid peroxidation in vitro; this suggests that neutrophils or macrophages are involved in LPS-induced lipid peroxidation.     

饮水中四氯化碳短期暴露健康风险参考值的验证

目的 针对四氯化碳的饮水短期暴露健康参考值的实验验证工作。方法 雄性SD大鼠分为6组（0、10、20、40、80、160 mg/（kg·d））,每组10只,玉米油作为阴性对照组。受试物组灌胃给予CCl4。染毒开始后24 h、11 d各组取5只大鼠,检测血清中OCT、SDH、ALT、AST、BUN。解剖取肝、肾进行组织病理学检查。结果 染毒24 h后,随着染毒剂量的增加,5项血清学指标均呈不同程度升高。大鼠体重、肝肾重及肝肾脏体比与阴性对照组相比均无明显变化。肝脏组织中观察到在80 mg/（kg·d）开始出现空泡。染毒11 d后,5项血清学指标均随着染毒剂量的增加而升高。各剂量组大鼠体重、肾重、肾脏体比与阴性对照组相比,均无明显变化。肝脏组织中观察到在20 mg/（kg·d）开始出现空泡,40 mg/（kg·d）起与对照组相比差异有统计学意义,随着剂量增加空泡病变严重。结论 本实验方案得出1 d的HA值为4 mg/L,10 d的HA值为1 mg/L,其中1 d的HA值与USEPA的相同,10 d的HA值比USEPA的高。     

Folate and vitamin B12 improved alcohol-induced hyperhomocysteinemia in rats

Objective

The purpose of this study was to investigate the protective effects of combined treatment of folate and vitamin B12 against alcoholic liver disease.

Methods

Male Wistar rats weighing about 160 g were divided into four groups: an ethanol group fed an ethanol liquid diet; a control group pair-fed an isoenergetic diet without ethanol; an ethanol and vitamin group fed an ethanol-containing diet that was supplemented with folate (10 mg/kg of body weight per day) and vitamin B12 (0.5 mg/kg of body weight per day); and a control and vitamin group fed an isoenergetic diet without ethanol, which was supplemented with folate (10 mg/kg of body weight per day) and vitamin B12 (0.5 mg/kg of body weight per day).

Results

After 16 wk, the plasma folate concentration in the ethanol group was significantly lower than in the other three groups. The plasma homocysteine concentration in the ethanol group was significantly higher than in the other three groups. The hepatic matrix metalloproteinase-2 concentration in the ethanol group was significantly higher than in the control and ethanol/vitamin groups. Furthermore, the plasma homocysteine concentration at the 16th week and the hepatic matrix metalloproteinase-2 concentration showed a significant positive correlation in rats of each group. In addition, pathologic evidence of liver fibrosis was observed only in the ethanol group. Furthermore, hepatic cytochrome 2E1 protein expression in group E increased significantly.

Conclusion

These results suggest that combined treatment of folate and vitamin B12 can alleviate alcoholic liver injury that may be related to normalization of plasma homocysteine levels.     

Maternal hepatic and embryonic effects of 1,2,4-trichlorobenzene in the rat

The possible maternal hepatic and reproductive effects of 1,2,4-trichlorobenzene (TCB) were assessed in rats given 0, 36, 120, 360, and 1200 mg/kg/day of TCB on Days 9-13 of gestation. The animals were sacrificed on Day 14 of pregnancy. Maternal deaths (2/9 rats, 6/6 rats) were recorded in the 360 and 1200 mg/kg/day treatment groups and body weight gain was significantly decreased in the 360 mg/kg/day TCB group. Maternal liver weight, liver/body weight ratio, and hepatic microsomal protein content were unaffected by TCB treatment. Although Day 14 NADPH-cytochrome c reductase activity was affected only at 360 mg/kg/day TCB, the maternal hepatic microsomal cytochrome P-450 content was significantly increased by administration of both 120 and 360 mg/kg/day of TCB. Hepatic microsomal aminopyrine N-demethylase, ethoxyresorufin O-deethylase, and UDP-glucuronyl transferase activity towards p-nitrophenol were also increased at 120 and 360 mg/kg TCB. Glutathione S-transferase activity to 1-chloro-2,4-dinitrobenzene and 1,2 dichloro-4-nitrobenzene were both increased by pretreatment with TCB. Although pretreatment with 360 mg/kg/day TCB did not increase resorptions, embryolethality, or teratogenicity, embryonic development was significantly retarded by all four growth criteria used (head length, crown-rump length, somite number, and protein content).     

Subacute effect of cigarette smoke exposure in rats: protection by pot marigold (Calendula officinalis L.) extract

This study was carried out to determine the preventive effect of Calendula officinalis L. (pot marigold) on rats exposed to cigarette smoke (CS). Rats were divided into three groups as control, CS and CS + pot marigold (PM). The rats in the CS and CS + PM groups were subjected to CS for 1 h twice a day for 23 days. PM (100 mg/kg body weight) was given to rats in the CS + PM group by gavage, 1 h before each administration period. While malondialdehyde, protein carbonyl contents and reduced glutathione level of the CS group increased, their levels diminished by PM administration. In addition, glutathione peroxidase (GPx), superoxide dismutase activities and β-carotene, vitamins A and C levels decreased in the CS group compared to control, however activities of these enzymes and concentration of vitamins were elevated by PM supplementation. This investigation showed that administration of PM supplied relative protection against subacute CS-induced cell injury.     

Pistacia lentiscus resin regulates intestinal damage and inflammation in trinitrobenzene sulfonic acid-induced colitis

Mastic (Pistacia lentiscus) of the Anacardiaceae family has exhibited anti-inflammatory and antioxidant properties in patients with Crohn's disease. This study was based on the hypothesis that mastic inhibits intestinal damage in inflammatory bowel disease, regulating inflammation and oxidative stress in intestinal epithelium. Four different dosages of P. lentiscus powder in the form of powder were administered orally to trinitrobenzene sulfonic acid-induced colitic rats. Eighty-four male Wistar rats were randomly assigned to seven groups: A, control; B, colitic; C-F, colitic rats daily supplemented with P. lentiscus powder at (C) 50 mg/kg, (D) 100 mg/kg, (E) 200 mg/kg, and (F) 300 mg/kg of body weight; and G, colitic rats treated daily with cortisone (25 μg/kg of body weight). Colonic damage was assessed microscopically. The cytokines tumor necrosis factor-α, intercellular adhesion molecule-1 (ICAM-1), interleukin (IL)-6, IL-8, and IL-10 and malonaldehyde were measured in colonic specimens. Results were expressed as mean ± SE values. Histological amelioration of colitis (P≤.001) and significant differences in colonic indices occurred after 3 days of treatment. Daily administration of 100 mg of P. lentiscus powder/kg of body weight decreased all inflammatory cytokines (P≤.05), whereas 50 mg of P. lentiscus powder/kg of body weight and cortisone treatment reduced only ICAM-1 (P≤.05 and P≤.01, respectively). Malonaldehyde was significantly suppressed in all treated groups (P≤.01). IL-10 remained unchanged. Cytokines and malonaldehyde remained unaltered after 6 days of treatment. Thus P. lentiscus powder could possibly have a therapeutic role in Crohn's disease, regulating oxidant/antioxidant balance and modulating inflammation.     

Effects of tocopherols and tocotrienols on body composition and bone calcium content in adrenalectomized rats replaced with dexamethasone

Long-term glucocorticoid treatment is associated with severe side effects, such as obesity and osteoporosis. A palm oil-derived vitamin E mixture had been shown previously to be protective against osteoporosis in rats given 120 microg/kg dexamethasone daily for 12 weeks. In this study we determined the effects of two isomers of vitamin E (i.e., palm oil-derived gamma-tocotrienol and the commercially available alpha-tocopherol, 60 mg/kg of body weight/day) on body composition and bone calcium content in adrenalectomized rats replaced with two doses of dexamethasone, 120 microg/kg and 240 microg/kg daily. Treatment period was 8 weeks. gamma-Tocotrienol (60 mg/kg of body weight/day) was found to reduce body fat mass and increase the fourth lumbar vertebra bone calcium content in these rats, while alpha-tocopherol (60 mg/kg of body weight/day) was ineffective. Therefore, in conclusion, palm oil-derived gamma-tocotrienol has the potential to be utilized as a prophylactic agent in prevention of the side effects of long-term glucocorticoid use.     

Ochratoxin A-induced apoptosis in rat kidney tissue

The aim of our study was to find whether ochratoxin A (OTA) induces the apoptosis and/or necrosis of kidney tissue in rats. In the first experiment, the highest number of apoptotic cells was found in rats sacrificed one day after OTA administration (1.00 mg/kg b.w., i.p.). The number of apoptotic cells reduced gradually and they were not seen nine days after OTA administration. A possible dose-dependence of histological changes was checked in kidney tissue of rats given 0.25, 0.50 or 1.00 mg of OTA/kg b.w., i.p. three times a week for four weeks. The number of apoptotic cells showed a clear dose-dependence, but necrosis was absent even at the highest doses. The time-dependent appearance of lesions related to OTA administration was checked by administering 0.50 mg OTA/kg body weight to rats, and sacrificing them one day after 1, 3, 6, and 9 doses/administrations, or 6 and 21 day after 12 doses/administrations. Long-term administration is associated with continued and increased apoptosis without necrosis, suggestive of OTA's role in the pathogenesis of progressive renal atrophy.     

NO2-/NO3- levels in blood and principal organs in rats treated with lipopolysaccharide

It is well revealed that activation of macrophages stimulated by endotoxin resulted in induction of nitric oxide synthase which catalyze nitric oxide (NO) formation from L-arginine. Consequently, blood concentrations of NO2-/NO3- (NOx-) are shown to increase. We studied on pharmaco/toxicokinetics of NOx- in serum and principal organs in Wistar male rats after i.p. administrations of LPS and NaNO3. The serum levels of NOx- at 1 h and 6 h after nitrate administration (10 mg/kg, i.p.) were 240 and 120 microM, respectively. Tissue levels of NOx- in lung, liver and kidneys were ca.1/2 of the serum level. Those levels in spleen and brain were ca.1/4 and 1/10 of the serum level, respectively. The correlation of NOx- levels in serum and these 5 organ tissues between 1 h and 6 h after administration of nitrate was r = 0.992 suggesting no specific accumulation of NOx- in these organs. The serum level of NOx- at 18 h after LPS treatment (1 mg/kg, i.p.) was 430 microM. The correlation of NOx- levels in serum and 5 organ tissues between LPS and nitrate administrations was shown to be r = 0.851. NOx- levels of serum, lung, kidneys and brain showed good correlation but liver and spleen showed out of the correlation. The liver tissue level of NOx- after LPS treatment was low compared with the expected value from the serum level. The reason may be explained partially by the liver weight increase and the liver toxicity with increased GPT and gamma-GT levels due to LPS. Contrary to this, NOx- level of spleen tissue after LPS treatment was more than 2-fold compared with the expected value from the serum level suggesting NO formation in the spleen. This was supported by the markedly high concentration (73.2 nmol/g tissue) of NO2- in the spleen tissue. NO2- levels in lung (34.5 nmol/g tissue) and brain (14.3) were also found to be significantly high after stimulation with LPS suggesting NO formation in these organs. Increased formation of NO2- in these organs by LPS stimulation suggests the formation of active nitrogen oxides such as N2O3 which is an effective nitrosating agent in non-acidic conditions in vivo.     

Effects of Picrorrhiza rhizoma water extracts on the subacute liver damages induced by carbon tetrachloride

The hepatoprotective activity of Picrorrhiza rhizoma (PR) water extract was evaluated on carbon tetrachloride (CCl(4))-induced subacute hepatic damage, induced by subcutaneous injection of CCl(4) (0.15 mL/kg of body weight) in pure olive oil (7.92%, vol/vol) three times a week for 10 weeks. Animals were sacrificed 10 weeks after oral administration of PR extracts at 50, 100, or 200 mg/kg or silymarin at 100 mg/kg, which were administered simultaneously with CCl(4); changes in body weight, liver weight, and serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were observed along with differences in liver histopathology and histomorphometry. In addition, liver malondialdehyde as an index for lipid peroxidation, hydoxyproline as an index for collagen synthesis, and protein content were determined. Ten weeks of CCl(4) injections caused subacute hepatic damage, featuring significantly less body weight gain and hepatic protein contents and higher liver weight, serum AST and ALT levels, and hepatic malondialdehyde and hydroxyproline contents with subacute hepatic damage-related histopathology of the liver. However, the CCl(4)-induced toxic effects were dramatically and dose-dependently inhibited by PR extract treatment. Thus oral administration of PR extracts significantly reduced CCl(4)-induced subacute hepatic damage in rats, probably by exerting a protective effect against hepatocellular necrosis via its free radical scavenging ability.     

Antihepatotoxic nature of Ulva reticulata (Chlorophyceae) on acetaminophen-induced hepatoxicity in experimental rats

Ulva reticulata, a marine edible green alga, is a known source of proteins, vitamins, and sulfated polysaccharides. Though there are many reports in the literature regarding the composition and antiviral property of Ulva sp., studies of the antihepatotoxic property of green seaweeds in animal model are scarce. We have studied the antihepatotoxic nature of this marine green edible alga, U. reticulata, in a hot water extract (150 mg/kg of body weight for a period of 15 days) against acetaminophen- induced hepatotoxicity in experimental albino rats. The acetaminophen-induced rats showed significant elevation in levels of the serum marker enzymes aspartate transaminase and alanine transaminase and of lipid peroxides in liver tissue with decreased levels of antioxidant enzymes such as superoxide dismutase and catalase. The levels of reduced glutathione and vitamins (E and C) were also decreased in the liver tissue of acetaminophen-intoxicated rats. The oral pretreatment with a hot water extract of U. reticulata reduced the hepatotoxicity triggered by acetaminophen considerably by improving the antioxidant status in experimental animals with depleted levels of lipid peroxides. These results indicate that the oral pretreatment with a hot water extract of U. reticulata in rats is effective in reducing the hepatic oxidative stress via free radical scavenging properties, suggesting an antihepatotoxic activity.     

亚硒酸钠与核黄素联合暴露对高脂饮食大鼠血脂及血清肝生化指标的影响

目的研究亚硒酸钠与核黄素联合暴露对高脂饮食雄性大鼠血脂及血清肝生化指标的影响。方法将60只健康SPF级雄性SD大鼠按体重随机分为空白对照组(10只)和高脂组(50只),分别给予基础饲料和高脂饲料;喂养4周后,将50只高脂组大鼠按照血脂水平和体重随机分为5组,分别为高脂对照组、1.84μg/kg亚硒酸钠+0.70 mg/kg核黄素干预组、18.40μg/kg亚硒酸钠+0.70 mg/kg核黄素干预组、1.84μg/kg亚硒酸钠+3.50 mg/kg核黄素干预组和18.40μg/kg亚硒酸钠+3.50 mg/kg核黄素干预组,每组10只。采用灌胃方式进行染毒,同时,空白对照组和高脂对照组给予相同体积的生理盐水,染毒容量为10 ml/kg,每天1次,连续60 d。分别于第0(染毒前)、20、40、60天,测定大鼠血清中总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)和高密度脂蛋白胆固醇(HDL-C)水平;并于第60天,检测大鼠血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转氨酶(AST)的水平。结果与空白对照组比较,染毒期间高脂对照组及各干预组大鼠血清TC、TG、LDL-C的水平均升高,除第60天时1.84μg/kg亚硒酸钠+0.70 mg/kg核黄素干预组大鼠血清TG水平外,差异有统计学意义(P0.05);而血清HDL-C水平均未见显著变化。与高脂对照组相比,第20、40天时1.84μg/kg亚硒酸钠+0.70mg/kg核黄素干预组大鼠血清TC、TG的水平及1.84μg/kg亚硒酸钠+3.50 mg/kg核黄素干预组大鼠血清TG的水平以及第60天时1.84μg/kg亚硒酸钠+0.70 mg/kg核黄素干预组大鼠血清TC、TG、LDL-C的水平及18.40μg/kg亚硒酸钠+0.70mg/kg核黄素干预组大鼠血清TC的水平均下降,差异有统计学意义(P0.05);而各干预组大鼠血清HDL的水平均无明显改变。与空白对照组比较,高脂对照组、18.40μg/kg亚硒酸钠+0.70 mg/kg核黄素干预组和1.84μg/kg亚硒酸钠+3.50mg/kg核黄素干预组大鼠血清ALT的水平以及高脂对照组、18.40μg/kg亚硒酸钠+0.70 mg/kg核黄素干预组和18.40μg/kg亚硒酸钠+3.50 mg/kg核黄素干预组大鼠血清AST的水平均升高,差异有统计学意义(P0.05)。与高脂对照组相比,仅1.84μg/kg亚硒酸钠+0.70 mg/kg核黄素干预组大鼠血清ALT的水平降低,差异有统计学意义(P0.05);1.84μg/kg亚硒酸钠+0.70 mg/kg核黄素干预组、18.40μg/kg亚硒酸钠+0.70 mg/kg核黄素干预组以及1.84μg/kg亚硒酸钠+3.50 mg/kg核黄素干预组大鼠血清AST的水平降低,差异均有统计学意义(P0.05)。结论适量亚硒酸钠与核黄素联合暴露可以拮抗高脂饮食所致雄性大鼠血脂及血清肝生化指标的升高。     

Maternal hepatic effects of 1,2,4,5-tetrachlorobenzene in the rat

1,2,4,5-Tetrachlorobenzene (TCB) is an industrial intermediate used in the production of 2,4,5-trichlorophenoxyacetic acid. This herbicide contains trace quantities of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Because of possible maternal hepatic or reproductive effects of this uncharged, low-molecular weight, lipophilic chlorinated benzene 0, 30, 100, 300, and 1000 mg/kg/day of TCB was orally administered to rats on Days 9, 10, 11, 12, and 13 of gestation and the animals were sacrified on Day 14 of pregnancy. No maternal deaths were recorded and body weight gain was significantly decreased only in the 1000 mg/kg/day group. Maternal liver weight, liver to body weight ratio, and hepatic microsomal protein content were unaffected by TCB treatment. Although Day 14 NADPH-cytochrome c reductase activity was not affected, the maternal hepatic microsomal cytochrome P-450 content was significantly increased by administration of 1000 mg/kg/day of TCB. Microsomal N-demethylation of aminopyrine was slightly increased from 2.4 to 3.4 and 3.5 nmole/mg protein/min at doses of 300 and 1000 mg/kg TCB. However, maternal hepatic microsomal ethoxyresorufin O-deethylase activity was greatly increased from 14 to 30, 40, 50, and 49 pmole/mg protein/min in pregnant rats administered 0, 30, 100, 300, and 1000 mg/kg/day TCB. The microsomal rates of p-nitrophenol and phenolphthalein glucuronidation in vitro were not increased by TCB administration. The maternal hepatic microsomal enzyme induction observed after TCB administration to pregnant rats suggests the presence both cytochrome P-450 and P-448 inducers in the sample of 1,2,4,5-tetrachlorobenzene used.