The Effects of Flaxseed Oil on Cadmium-Induced Oxidative Stress in Rats

In the present study, the effects of flaxseed oil on the oxidant–antioxidant system in cadmium intoxication were investigated in rats. Forty-eight male Wistar albino rats were divided into four equal groups (group 1). No treatment was applied to the control group. On the other hand, groups 2, 3, and 4 were administered with 0.1 ml/rat/day (～500 mg/kg bw) flaxseed oil by gavage into the stomach, 50 ppm of cadmium (～4 mg/kg bw) in ad libitum drinking water, and 0.1 ml/rat/day flaxseed oil plus 50 ppm of cadmium, respectively, for 30 days. At the end of the study, malondialdehyde and nitric oxide levels and catalase, superoxide dismutase, and glutathione peroxidase activities were measured in blood and tissue (liver, lung, kidney, brain, heart, and testes) samples. While malondialdehyde and nitric oxide levels increased in the group given cadmium compared to the control group; in the meantime, there were some significant changes in antioxidant enzyme activities. These changes were observed, the trends of decrease or increase compared to the control group. There were positive changes in parameters of the group given with flaxseed oil plus cadmium compared to the group receiving cadmium alone, in other words, values were seen coming close to control group. As a result, cadmium exposure caused oxidative damage to erythrocytes and organs at varying rates, while flaxseed oil reduced the severity of cadmium-induced lipid peroxidation. Therefore, it was concluded that flaxseed oil can be used among compounds as a therapeutic agent or food additive for prophylaxis in cadmium intoxication.     

Effects of Flaxseed Oil on Lead Acetate-Induced Neurotoxicity in Rats

It is well known that chronic exposure to lead (Pb(+2)) alters a variety of behavioral tasks in rats and mice. Here, we investigated the effect of flaxseed oil (1,000?mg/kg) on lead acetate (20?mg/kg)-induced brain oxidative stress and neurotoxicity in rats. The levels of Pb(+2), lipid peroxidation, nitric oxide (NO), and reduced glutathione (GSH) and the activity of catalase (CAT), superoxide dismutase (SOD), glutathione reductase (GR), glutathione-S-transferase (GST), and glutathione peroxidase (GPx) were determined in adult male albino rats. The level of Pb(+2) was markedly elevated in brain and blood of rats. This leads to enhancement of lipid peroxidation and NO production in brain with concomitant reduction in GSH, CAT, SOD, GR, GST, and GPx activities. These findings were associated with DNA fragmentation. In addition, lead acetate induced brain injury as indicated by histopathological changes of the brain. Treatment of rats with flaxseed oil resulted in marked improvement in most of the studied parameters as well as histopathological features. These findings suggest to the conclusion that flaxseed oil significantly decreased the adverse harmful effects of lead acetate exposure on the brain as well as Pb(+2)-induced oxidative stress.     

Flaxseed Oil as a Neuroprotective Agent on Lead Acetate-Induced Monoamineric Alterations and Neurotoxicity in Rats

Lead remains a considerable occupational and public health problem, which is known to cause a number of adverse effects in both man and animals. Here, the neuroprotective effect of flaxseed oil (1,000 mg/kg) on lead acetate (20 mg/kg) induced alternation in monoamines and brain oxidative stress was examined in rats. The levels of lead, dopamine (DA), norepinephrine (NE), serotonin (5-HT), lipid peroxidation, nitrite/nitrate (NO), and glutathione (GSH) were determined; also, the activity of acetylcholinesterase (AChE) and Na(+)-K(+)-ATPase were estimated on different brain regions of adult male albino rats. The level of lead was markedly elevated in different brain regions of rats. This leads to enhancement of lipid peroxidation and NO production in brain with concomitant reduction in AChE activity and GSH level. In addition, the levels of DA, NE, and 5-HT were decreased in the brain. These findings were associated with BAX over expression. Treatment of rats with flaxseed oil induced a marked improvement in most of the studied parameters as well as the immunohistochemistry features. These data indicated that dietary flaxseed oil provide protection against lead-induced oxidative stress and neurotoxic effects.     

Lead-Induced Hearing Loss in Rats and the Protective Effect of Copper

Lead is a common environmental pollutant which can induce various toxic effects to humans and/or animals. This work aimed to study the hearing loss in rats induced by lead and the protective effect of copper. The auditory brainstem response (ABR) was used to study the hearing loss in rats. The results showed that lead prolonged the latencies of wave I to V of ABRs of the rats but did not affect the interpeak latencies of waves I-III, III-V, and I-V, indicating that lead could cause hearing loss in rats by impairing the cochlea. After receiving copper, the quality and the wave latencies of the ABR of the rats were restored to a certain extent, indicating that copper played a protective role in lead-induced hearing impairment. The mechanisms were also proposed that lead could cause hearing loss in rats mainly through damaging the cochlea component, and copper might antagonize the toxicity of lead in three primary ways.     

Protective Effect of Naringenin Against Lead-Induced Oxidative Stress in Rats

Oxidative stress is thought to be involved in lead-induced toxicity. The aim of this study was to investigate the possible protective role of naringenin on lead-induced oxidative stress in the liver and kidney of rats. In the present investigation, lead acetate (500 mg Pb/L) was administered orally for 8 weeks to induce hepatotoxicity and nephrotoxicity. The levels of hepatic and renal markers such as alanine aminotransferase, aspartate aminotransferase, urea, uric acid, and creatinine were significantly (P < 0.05) increased following lead acetate administration. Lead-induced oxidative stress in liver and kidney tissue was indicated by a significant (P < 0.05) increase in the level of maleic dialdehyde and decreased levels of reduced glutathione, superoxide dismutase, catalase, and glutathione peroxidase. Naringenin markedly attenuated lead-induced biochemical alterations in serum, liver, and kidney tissues (P < 0.05). The present study suggests that naringenin shows antioxidant activity and plays a protective role against lead-induced oxidative damage in the liver and kidney of rats.     

Trypanosoma lewisi Infections in Normal Rats and in Rats Treated with Dexamethasone

SYNOPSIS. Administration of dexamethasone to rats infected with Trypanosoma lewisi resulted in the development of exceedingly large populations of trypanosomes which were fatal to their hosts. The elevated levels of parasitemia in treated rats early in infections were thought not to be a result of an increased reproductive rate. However, trypanosomes in treated rats 2 days postinfection did have a higher coefficient of variation in total length and a greater percentage of dividing forms than those observed from infected rats which were not given the drug. The course of infection may be markedly altered not only in intensity but also in length by this corticosteroid. It is suggested that dexamethasone administered at the levels recorded to rats infected with T. lewisi inhibits the production of ablastin and trypanocidal antibodies.     

The Protective Effects of Eugenol on Carbon Tetrachloride induced Hepatotoxicity in Rats

Our earlier studies in vitro have shown that eugenol inhibits liver microsomal monooxygenase activities and carbon tetrachloride (CCl₄)-induced lipid peroxidation (Free Rad. Res. 20,253-266,1994). The objective of the present investigation was to study the in vivo protective effect of eugenol against CCI₄ toxicity. Eugenol (5 or 25 mg/kg body wt) given orally for 3 consecutive days did not alter the levels of serum glutamic oxalacetic transaminase (SGOTJ, microsomal enzymes such as cytochrome P450 reductase, glucose-6-phosphatase (G-6-Pase) xenobiotic-metabolizing enzymes (aminopyrine-N-demethylase, N-nitrosodimethylamine-demethylase and ethoxyresorufin-O-deethylase) and liver histology. Doses of eugenol (5 or 25 mg/kg) administered intragastrically to each rat on three consecutive days i.e. 48 hr, 24 hr and 30 min before a single oral dose of CCU (2.5 ml/kg body wt) prevented the rise in SGOT level without appreciable improvement in morphological changes in liver. Eugenol pretreatment also did not influence the decrease in microsomal cytochrome P₄₅₀ content, G-6-Pase and xenobiotic-metabolizing enzymes brought about by CCI₄. Since eugenol is metabolized and cleared rapidly from the body, the dose schedule was modified in another experiment. Eugenol (0.2,1.0,5.0 or 25 mg/kg) when given thrice orally i.e. prior to (-1 hr) along with (0 hr) and after (+ 3 hr) the i.p. administration of CCI₄ (0.4 ml/kg) prevented significantly the rise in SGOT activity as well as liver necrosis. The protective effect was more evident at 1 mg and 5 mg eugenol doses. However, the decrease in microsomal G-6-Pase activity by CCI₄ treatment was not prevented by eugenol suggesting that the damage to endoplasmic reticulum is not protected. The protective effect of eugenol against CC1₄ induced hepatotoxicity is more evident when it is given concurrently or soon after rather than much before CCU treatment.     

Bioelement Status with Oral Administration of Fish Oil Methyl Ester and Diesel Fuel in Male Rats

This paper is a study on the effects on the amounts of trace elements in case of possible repeat accidental or environmental exposure with fish oil biodiesel. For this purpose, 35 male Wistar albino rats were used in the study. Rats were divided into five groups. The first group was determined as the control group. The rats in this group were gavaged orally with 250?mg/kg sunflower oil. The rats in the second and third groups were administered by oral gavage of 250?mg/kg (D1) and 500?mg/kg (D2) diesel fuel mixed with equal amounts of sunflower oil, respectively. The rats in the fourth group were administered by oral gavage of 250?mg/kg fish oil biodiesel (F1) and the rats in the fifth group were administered by oral gavage of 500?mg/kg fish oil biodiesel (F2), both mixed with equal amounts of sunflower oil. At the end of the study, bioelement concentrations in the serum and the kidney, lung, and liver tissues were measured using inductively coupled plasma-optical emission spectroscopy. It was observed that serum Ca, Mg, and Sr concentrations were significantly (p?相似文献   

Anti-Proliferative Activities of Sinigrin on Carcinogen-Induced Hepatotoxicity in Rats

Liver cancer is one of the leading causes of cancer death worldwide. A very high incidence of new liver cancer cases is diagnosed every year, and metastasis has been found to correlate to poor prognoses in humans. Better treatments for liver cancer are thus clearly needed. Sinigrin is one of the major ingredients present in Brassica nigra, which has been used in combination with other herbs for treatment of various diseases. The anti-proliferative activities of sinigrin were studied in a model of carcinogen-induced hepatotoxicity in rats. Rats were orally administered with sinigrin on a daily basis for three months before sacrifice. Sinigrin was found to significantly inhibit the proliferation of liver tumor cells; the number of surface tumors in the rat liver was dramatically reduced. Sinigrin induced apoptosis of liver cancer cells through up-regulation of p53 and down-regulation of Bcl-2 family members and caspases. Our findings indicated that the liver functions were gradually restored after treatment with sinigrin and that the agent did not cause liver toxicity. Cell cycle analysis indicated that sinigrin caused cell cycle arrest in G0/G1 phase. The results suggest that sinigrin exerts important anti-proliferative activities in carcinogen-induced hepatocarcinogenesis in rats, and highlight the potential of sinigrin as an anti-cancer agent for liver cancer.     

Chronic Manganese Administration with Longer Intervals Between Injections Produced Neurotoxicity and Hepatotoxicity in Rats

Neurochemical Research - Subacute exposure to manganese (Mn) produced Parkinson’s disease-like syndrome called Manganism. Chronic onset and progression are characteristics of Manganism,...     

环境胁迫和抗坏血酸的氧化还原状态

为了解环境胁迫对植物体中抗坏血酸含量及氧化还原状态的影响，以不同强度的冰冻和干旱两种胁迫为例，研究了它们对沈阳几种针叶树离体叶抗坏血酸、脱氢抗坏血酸含量以及抗坏血酸-谷胱甘肽循环中4种酶活性的影响。结果表明，两种胁迫达到一定强度后，都能使还原态抗坏血酸含量下降而使脱氢抗坏血酸含量上升。冰冻使抗坏血酸过氧化酶和单脱氢抗坏血酸还原酶活性下降。轻度失水使这两种酶活性上升，失水加重后转而趋于下降。脱氢抗坏血酸还原酶和谷胱甘肽还原酶活性对两种胁迫反应均不如前两种酶敏感。结合以前的研究结果，认为这一H2O2清除系统在导致驯化(acclimation)的轻度胁迫作用下可以得到加强，而当胁迫强度过大时则其清除能力下降并使组织受到伤害。文中还报告了沈阳几种针叶树抗寒性和针叶中抗坏血酸含量及上述4种酶活性之间的相关关系。     

The Distribution of Serotonergic Nerves in Microencephalic Rats Treated Prenatally with Methylazoxymethanol

Prenatal exposure of pregnant rats to methylazoxymethanol acetate (MAM) induces microencephaly in the offspring. In the present study of these microencephalic rats (MAM rats) we used quantitative autoradiography to investigate [³H] paroxetine binding sites, which are a selective marker of serotonin (5-HT) transporters (5-HTT). The binding in the accumbens, cortex, hippocampus, and dorsolateral thalamus was significantly increased in MAM rats, compared to the control rats, while there was a significant decrease in the dorsal raphe nucleus of the MAM rats. The levels of 5-HTT mRNA in the dorsal raphe nuclei were analyzed by in situ hybridization, which revealed a significant decrease in 5-HTT mRNA-positive neurons in the MAM rats compared to the control rats. The results imply serotonergic hyperinnervation in the cerebral hemispheres of MAM rats, while a target-dependent secondary degeneration of 5-HT neurons might be induced in the dorsal raphe nuclei of MAM rats.     

Protective Effects of Garlic and Silymarin on NDEA-Induced Rats Hepatotoxicity

Background ­— The present study was conducted to investigate the chemopreventive effects of garlic extract and silymarin on N-nitrosodiethylamine (NDEA) and carbon tetrachloride (CCl₄)-induced hepatotoxicity in male albino rats. Methods and Results — Animals were pretreated with garlic, silymarin or both for one week prior to the injection of NDEA. Then animals received a single injection of NDEA followed by weekly subcutaneous injections of CCl₄ for 6 weeks. Oral administration was then continued along with the injection of CCl₄ for the duration of the experiment. Serum aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), hepatic lipid peroxidation (LPO), superoxide dismutase (SOD), reduced glutathione (GSH), glutathione-S-transferase (GST) and glutathione reductase (GSR) were measured. Injection of NDEA induced a significant elevation in serum AST, ALT and ALP. In the liver, NDEA increased oxidative stress through the increase in LPO and decrease in SOD, and GSH-dependent enzymes. Although administration of garlic or silymarin significantly reduced the liver toxicity, combined administration was more effective in preventing the development of hepatotoxicity. Conclusion — These novel findings suggest that silymarin and garlic have a synergistic effect, and could be used as hepatoprotective agents against hepatotoxicity.     

Ferulic Acid Modulates Fluoride-Induced Oxidative Hepatotoxicity in Male Wistar Rats

The present study is aimed to evaluate the protective effect of ferulic acid (FA) on fluoride-induced oxidative hepatotoxicity in male Wistar rats. Fluoride (25 mg/L) was given orally to induce hepatotoxicity for 12 weeks. Hepatic damage were assessed using status of pathophysiological markers like serum marker enzymes like aspartate transaminase, alanine transaminase, alkaline phosphatase, acid phosphatase, gamma glutamyl transferase, lactate dehydrogenase, bilirubin, lipid profile, total protein content levels, and histopathological studies. Treatment with FA significantly reduced the degree of histological abberations and rescued lipid peroxidation, as observed from reduced levels of lipid hydroperoxides, nitric oxide, restored levels of enzymic and non-enzymic antioxidants, and total protein content, with a concomitant decline in the levels of marker enzymes and lipid profile in fluoride-induced rats. These results suggest that ferulic acid has the ability to protect fluoride-induced hepatic damage.     

环境胁迫和抗坏血酸的氧化还原状态

为了解环境胁迫对植物体中抗坏血酸含量及氧化还原状态的影响,以不同强度的冰冻和干旱两种胁迫为例,研究了它们对沈阳几种针叶树离体叶抗坏血酸、脱氢抗坏血酸含量以及抗坏血酸-谷胱甘肽循环中4种酶活性的影响.结果表明,两种胁迫达到一定强度后,都能使还原态抗坏血酸含量下降而使脱氢抗坏血酸含量上升.冰冻使抗坏血酸过氧化酶和单脱氢抗坏血酸还原酶活性下降.轻度失水使这两种酶活性上升,失水加重后转而趋于下降.脱氢抗坏血酸还原酶和谷胱甘肽还原酶活性对两种胁迫反应均不如前两种酶敏感.结合以前的研究结果,认为这一H2O2清除系统在导致驯化(acclimation)的轻度胁迫作用下可以得到加强,而当胁迫强度过大时则其清除能力下降并使组织受到伤害.文中还报告了沈阳几种针叶树抗寒性和针叶中抗坏血酸含量及上述4种酶活性之间的相关关系.     

Salidroside Protects against Cadmium-Induced Hepatotoxicity in Rats via GJIC and MAPK Pathways

It is known that cadmium (Cd) induces cytotoxicity in hepatocytes; however, the underlying mechanism is unclear. Here, we studied the molecular mechanisms of Cd-induced hepatotoxicity in rat liver cells (BRL 3A) and in vivo. We observed that Cd treatment was associated with a time- and concentration-dependent decrease in the cell index (CI) of BRL 3A cells and cellular organelle ultrastructure injury in the rat liver. Meanwhile, Cd treatment resulted in the inhibition of gap junction intercellular communication (GJIC) and activation of mitogen-activated protein kinase (MAPK) pathways. Gap junction blocker 18-β-glycyrrhetinic acid (GA), administered in combination with Cd, exacerbated cytotoxic injury in BRL 3A cells; however, GA had a protective effect on healthy cells co-cultured with Cd-exposed cells in a co-culture system. Cd-induced cytotoxic injury could be attenuated by co-treatment with an extracellular signal-regulated kinase (ERK) inhibitor (U0126) and a p38 inhibitor (SB202190) but was not affected by co-treatment with a c-Jun N-terminal kinase (JNK) inhibitor (SP600125). These results indicate that ERK and p38 play critical roles in Cd-induced hepatotoxicity and mediate the function of gap junctions. Moreover, MAPKs induce changes in GJIC by controlling connexin gene expression, while GJIC has little effect on the Cd-induced activation of MAPK pathways. Collectively, our study has identified a possible mechanistic pathway of Cd-induced hepatotoxicity in vitro and in vivo, and identified the participation of GJIC and MAPK-mediated pathways in Cd-induced hepatotoxicity. Furthermore, we have shown that salidroside may be a functional chemopreventative agent that ameliorates the negative effects of Cd via GJIC and MAPK pathways.     

Effect of Porcine Placental Extract Mixture on Alcohol-Induced Hepatotoxicity in Rats

This study was conducted to examine the effect of porcine placenta extract mixture (pPEM, enzymatic/acidic extract = 1/3) on alcoholic hepatotoxicity after pPEM dosing with alcohol in rats. The experimental groups were normal, control, silymarin, three pPEM (590, 1771, and 2511 mg/kg/day, po), and silymarin (100 mg/kg/day, po) groups (n = 10). Alcoholic hepatotoxicity was caused by a liquid ethanol diet for 4 weeks. The effect of pPEM and silymarin on alcoholic hepatotoxicity was evaluated by serology, hepatic ADH and ALDH activities, and histopathological findings. After oral dosing with alcohol for 4 weeks, ALT and AST were significantly increased to 33.7 → 115.6 and 81.37 → 235.0 in the alcohol group, respectively. These levels were decreased significantly to 83.9 and 126.7 in the silymarin group and dose-dependently to 73.6–56.9 and 139.2–122.8 in all pPEM groups. Hepatic ADH and ALDH might have been increased in the control and not in the silymarin and pPEM groups for hepatic ADH. All pPEM groups exhibited no effects on hepatic ALDH except for the high pPEM group. Mild inflammation and fatty lesions were observed in the alcohol group and were attenuated in the silymarin and pPEM groups. As a results, the pPEM showed protective activities against alcoholic hepatotoxicity on the serological markers, hepatic ADH and ALDH, and pathological findings.     

Flaxseed Oil for Control of Peanut Rust and Its Disease Control Mechanism

Severity of peanut rust caused by Puccinia arachidis was reduced by 15 edible oils tested. Flaxseed oil was the best suppressing the disease completely. Peanut oil, wheat germ oil, brown rice oil, aloe oil, olive oil and corn germ oil also caused more than 75% reduction in disease incidence. Flaxseed oil reduced the rust to a negligible level in the greenhouse and was nearly as effective as the fungicide chlorothalonil in peanut field trials. The control of peanut rust by flaxseed oil did not result from activation of the host defence mechanisms. Flaxseed oil did not affect urediniospore germination, but reduced the germ tube length and completely suppressed appressorium formation which is essential for the pathogen to form an infection peg to pass through the stomatal aperture and infect the host tissue. Although the pathogen had penetrated, flaxseed oil still exerted some inhibitory effect against the growth of the pathogen. The advantages of using flaxseed oil to control peanut rust are that it is relatively inexpensive, easy to prepare, and friendly to the environment and human health.