Free Radicals In Liver Research Articles

Comparative studies of influence of palm oil on activity of xanthine oxidase and free radicals in liver and blood: Diabetes and metabolic syndrom

Diabetes is a chronic metabolic disease, which has affected approximately 10.5% of the global population [1]. The most frequent types of diabetes are type-1 and type-2. The third frequent type is gestational diabetes. The pathogenicity of diabetes is multifactorial and involves various factors such as genetic, food, stress, environmental pollutants, and others, in most of the cases combination of two or more factors are noticed. Comparative studies of the influence of palm oil on the activity of xanthine oxidase (XOD) and free radicals in liver and blood. The research compared the effect of palm oil on carbohydrate metabolism in male rats: in young rats and adult rats. The research compared the effect of palm oil on free radicals in male rats: in adults and juvenile rats. Experimental animal body weight change research, 30 days after palm oil treatment. For this scientific research we utilized experimental animals of the male genus: mice of the Wistar type, small mice (45-60 g) and large mice (160-180 g). Experimental animals were divided into groups of six-eight experimental mice and details are shown in the corresponding part of the results. The results are shown in six figures and two tables. Results indicate an increase in the formation of free radicals in blood plasma, both in experimental juvenile mice and in experimental large mice under the influence of palm oil. Palm oil increases the activity of XOD in blood, both in small animals and in large experimental animals. Palm oil increases the formation of XOD in the black liver in both elderly groups. In all groups during the experiment there was an increase in body weight. Results from studies of the effect of palm oil on carbohydrate metabolism showed changes in glucose tolerance test. Current studies for the first time convincingly demonstrate the risk of using palm oil. Analysis of the results of two studies on XOD and carbohydrate metabolism showed a correlation between increased XOD levels and the development of prediabetes.

Oxidative stress and free radicals in liver and kidney diseases; an updated short-review

Context: In normal conditions, liver and kidney act as a supply of internal antioxidants for neutralizing free radicals produced by viruses and internal/external compounds which were processed in the liver and kidney. Evidence Acquisition: PubMed, EBSCO, Embase, Web of Science, directory of open access journals (DOAJ), Scopus, and Google Scholar were searched using keywords of oxidative stress, free radicals, liver diseases, kidney diseases and antioxidant therapy. Results: When the antioxidants of the liver or kidney are low, or when the liver/kidney is under pressure through oxidative insults, the damages produced by free radicals would increase, leading to inflammation and fibrosis. In addition to cytotoxic effect of oxidative stress, it has also a substantial role in modulating of messengers in regulating the functions of cell membrane, with a vital factor for survival. However, there is also some benefits of oxidative stress such as inducing apoptosis to prepare birth canal for delivery or strengthening of biological defense mechanisms during ischemia and physical exercise. Conclusions: There is an important association between diseases related to lifestyle and oxidative stress, as a condition that oxidation may exceed the antioxidant systems of the body with absence of balance between them. Oxidative stress is involved with many diseases such as kidney, liver and lung dysfunctions. Supplementation with vitamins C and E and selenium for four months could improve the balance between antioxidant-oxidant as well as potential slowing down of liver disease progression.

Evaluation of Methanol Induced Free Radicals in Mice Liver

Methanol induced oxidative stress (OS) models in mice were successfully established and evaluated by the electron paramagnetic resonance (EPR) spin trapping technique. The capacity for removal of reactive oxygen species (ROS) free radicals by rhubarb and vitamin C (Vc) as candidate materials was also investigated. EPR was employed to determine the free radicals generated from a spin trapping agent, α-phenyl-N-tert-butylnitrone (PBN), that reacted with the ROS. The activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX), and the level of malondialdehyde (MDA) were also evaluated by enzyme assays. The results indicated that methanol clearly promoted the generation of ROS free radicals in the liver of mice. The activity of SOD and GSH-PX was reduced significantly, although the level of MDA was increased as a result of the harmful effect of methanol. In addition, rhubarb and Vc exhibited a protective effect on the mice liver under acute OS.

Protective effects of penehyclidine hydrochloride on liver injury induced by cardiopulmonary bypass in Guangxi bama miniature pig

Objective To investigate the effects of penehyclidine hydrochloride on liver injury induced by cardiopulmonary bypass (CPB) in Guangxi bamaminiature pig.Methods Twenty-seven Bama miniature pigs weighted 32-40 kg were chosen,three pigs were used for sampling blood,another twentyfour pigs were used for cardiopulmonary bypass (CPB).Twenty-four pigs were randomly divided into three groups (n=8 each):group Sham,group Mod,and group PHC.Propofol,fentanyl and vecuronium were continued by intravenous injection and inhaled isoflurane interruptly for anesthesic maintain.CPB was performed on mild hypothermic beating heart for 120 min.Pnehyclidine hydrochloride 0.1 mg/kg was injected intravenously before 10 min CPB.Blood samples were collected for aspartate aminotransferase (AST),alanine transaminase (ALT),direct bilirubin (DB) and total bilirubin (TB) before CPB (T0),after CPB 1 h (T1),CPB cease (T2) and operation cease (T3).The content of ATP,MDA and SOD in liver tissue at befor and after CPB were measured and the pathologic change of liver was evaluated by electron microscope.Results The levels of ALT,AST,DB and TB in group Mod and group PHC were significantly higher at T1-T3 than those in group Sham (P ＜ 0.05).ATP,SOD were lower and MDA was higher significantly in group Mod and group PHC after CPB than that in group Sham (P ＜ 0.05).Compared with the group Mod,The levels of ALT,AST,DB,TB and MDA were lower and ATP,SOD were higher significantly respectively in group PHC (P ＜ 0.05).The electron microscopec examination showed that histologic damage was significantly reduced in group PHC compared with group Mod.Conclusion Pnehyclidine hydrochloride can attenuate Iiver injury induced by CPB,antioxygen to remove oxygen free radical in liver may be the mechanism. Key words: Penehyclidine hydrochloride ; Cardiopulmonary bypass ; Liver injury ; Antioxygen

Zinc supplement modulates oxidative stress and antioxidant values in rats with severe acute pancreatitis.

Oxidative stress is a main factor in the pathogenesis of severe acute pancreatitis (SAP). The ability of zinc (Zn) to retard oxidative processes has been recognized for many years. This study aims to examine the levels of free oxygen radicals and antioxidant enzyme in SAP rats and know the effect of Zn supplementation on free oxygen radicals and antioxidant system in rats with SAP. Forty-five male Wistar rats were divided into three groups-the SAP group (n=15), the Zn-treated group (n=15), and the controlled group (n=15). For the SAP group, sodium taurocholate is injected into the pancreatic duct to induce SAP; for the Zn-treated group, Zn (5 mg/kg) is subcutaneously injected immediately after injection of 5% sodium taurocholate. Firstly, the activity of erythrocyte glutathione peroxidase (GSH-Px), erythrocyte superoxide dismutase (SOD), and the content of plasma malondialdehyde (MDA), which are the toxic products of oxidative stress, is measured. Secondly, the levels of free oxygen radicals in the liver and kidney are detected. The result showed that the activity of GSH-Px and SOD was lower in the SAP group than that in the controlled group, although the content of plasma MDA increased. However, the activity of SOD and GSH-Px in the Zn-treated group was not significantly decreased after comparing with the controlled group; in the mean time, the content of MDA was not significantly increased either. Moreover, the content of free radical in liver and kidney was higher in the SAP group compared with the controlled group, but the content of free radical in the Zn-treated group was not higher than that in the controlled group (p>0.05). All of the above indicated that Zn may recover the activity of free radical-scavenging enzymes and decrease the content of free radical for the SAP group rats. In conclusion, the content of free radical increase may be one of the reasons that SAP rats are injured, and it is possible for Zn to be used to treat SAP through scavenging free radical and increasing the activity of SOD and GSH-Px of erythrocyte.

Immunomodulatory Effects of Danshen (Salvia miltiorrhiza) in BALB/c Mice

Danshen, the root and rhizome of Salvia miltiorrhiza Bge, a Traditional Chinese Medicine, especially for cardiovascular and cerebrovascular diseases, has unique immunomodulatory effects. Danshen is capable of anti-inflammation and antiallergy, which are immunosuppressive activities, whereas it is also able to promote immunity against cancer, viruses, and bacteria. Most previous reports were performed with use of a purified compound or compounds of Danshen. Since there are more than twenty active compounds in Danshen, it is very difficult to predict that one compound will act the same way when it is combined with other compounds. In order to overcome this limitation, we used the crude form of Danshen to study its immunomodulatory effects in a mouse model. The mice were fed daily diet supplements of Danshen for three months and then tested for their immunity, including leukocyte subsets in peripheral blood, humoral and cell-mediated immune responses, and host defenses against a Listeria monocytogenes (LM) infection. Different doses of Danshen caused different immunomodulatory effects. Danshen at 0.5% decreased serum IgE production in BALB/c mice; 1% Danshen promoted cell-mediated immunity; Danshen at 0.5 and 1% inhibited the production of oxygen free radicals in liver and spleen and NO production in liver; 2% Danshen enhanced the host resistance against LM with increased numbers of peripheral monocytes and natural killer (NK) cells and decreased production of IL-1β and NO.

The influence of short-term l-arginine supplementation on rats’ muscular and hepatic cells in ischemia–reperfusion syndrome

Due to the complex mechanisms of L-arginine activity, it is difficult to determine the clinical significance of supplementation with this amino acid. The objective of this study was to determine the influence of short-term supplementation with L-arginine in stress conditions, induced by ischemia-reperfusion syndrome, by assessing the damage to muscular and hepatic cells on the basis of creatine kinase (CK), alanine aminotransferase (ALAT) and aspartic aminotransferase (AspAT) activity in blood and the level of oxygen free radicals in analyzed tissues of rats. We observed that induced ischemia of hind limb caused an increase in CK, ALAT and AspAT activity and an increase in the level of free radicals in liver, but not in skeletal muscle. Supplementation with L-arginine led to a reduction in serum activity of CK and AspAT and reduction of the level of free radicals in analysed tissues. Simultaneous supplementation with L -arginine AND L-NAME resulted in a reversal of changes induced by L-arginine supplementation in the case of AspAT and free radicals in skeletal muscle. The results indicate that under conditions of ischemia-reperfusion, short-term administration of L-arginine has a protective effect on skeletal muscle manifesting itself by reduction of CK in the serum and reduction of free radicals level in THIS tissue.

Biochemical Study on the Protective Role of Folic Acid in Rabbits Treated with Chromium (VI)

Deleterious effects of chromium (VI) compounds are diversified affecting almost all the organ systems in a wide variety of animals. Therefore, the present study was carried out to determine the effectiveness of folic acid (FA) in alleviating the toxicity of chromium (VI) on certain biochemical parameters, lipid peroxidation, and enzyme activities of male New Zealand white rabbits. Six rabbits per group were assigned to one of four treatment groups: 0 mg FA and 0 mg Cr(VI)/kg BW (control); 8.3 μg FA/kg BW; 5 mg Cr(VI)/kg BW; 5 mg Cr(VI) plus 8.3 μg FA/kg BW, respectively. Rabbits were orally administered their respective doses every day for 10 weeks. Results obtained showed that Cr(VI) significantly (P < 0.05) increased the levels of free radicals and the activity of glutathione S-transferase (GST), and decreased the content of sulfhydryl groups (SH groups) in liver, testes, brain, kidney, and lung. The activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AlP), acid phosphatase (AcP), and lactate dehydrogenase (LDH) were significantly decreased in liver and testes due to Cr(VI) administration. Also, AlP and AcP activities were significantly decreased in kidney and lung. The activity of acetylcholinesterase (AChE) was significantly decreased in brain and plasma. Contrariwise, the activities of AST and ALT were significantly increased in plasma, while AlP and AcP decreased. Chromium (VI) treatment caused a significant decrease in plasma total protein (TP) and globulin, and increased total lipids (TL), cholesterol, glucose, urea, creatinine, and bilirubin concentrations. Folic acid alone significantly decreased the levels of free radicals in liver, brain, and kidney, and increased the content of SH-group. The activities of AST, ALT, and LDH in liver; AST, ALT, AlP, AcP, and LDH in testes; AcP in kidney; AlP and AcP in lung, and LDH in brain were significantly increased. Plasma TP and albumin were increased, while urea and creatinine were decreased. The presence of FA with Cr(VI) restored the changes in enzyme activities and biochemical parameters. In conclusion, folic acid could be effective in the protection of chromium-induced toxicity.

Effects of D-amino acids on lipoperoxidation in rat liver and kidney mitochondria

The effects of the amino acids D-ser, D-asp, and D-ala on lipoperoxidation under conditions of hypertension, alcoholism, and ammonemia in rat liver and kidney mitochondria were studied. Under normal conditions, D-alanine increased in 54% free radicals production in liver mitochondria (p < 0.05). The D-amino acids had no effect on kidney mitochondria. D-ser and D-ala increased lipoperoxidation in spontaneously hypertensive rats (SHR) as compared with their normotensive genetic control Wistar-Kyoto (WKY) rats (p < 0.05). During hypertension and in oxidative stress in the presence of calcium, only D-ala produced 46% and 29% free radicals in liver and kidney mitochondria (p < 0.05), respectively. During chronic alcoholism, D-ser increased lipoperoxidation in 80% in kidney mitochondria (p < 0.05), as compared to control. During ammonemia, D-ser produced 41% free radicals.

Phthalates rapidly increase production of reactive oxygen species in vivo: role of Kupffer cells.

The role of oxidants in the mechanism of tumor promotion by peroxisome proliferators remains controversial. The idea that induction of acyl-coenzyme A oxidase leads to increased production of H(2)O(2), which damages DNA, seems unlikely; still, free radicals might be important in signaling in specialized cell types such as Kupffer cells, which produce mitogens. Because hard evidence for increased oxidant production in vivo after treatment with peroxisome proliferators is lacking, the spin-trapping technique and electron spin resonance spectroscopy were used. Rats were given di(2-ethylhexyl) phthalate (DEHP) acutely. The spin trapping agent alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone was also given and bile samples were collected for 4 h. Under these conditions, the intensity of the six-line radical adduct signal increased to a maximum value of 2.5-fold 2 h after administration of DEHP, before peroxisomal oxidases were induced. Furthermore, DEHP given with [(13)C(2)]dimethyl sulfoxide produced a 12-line electron spin resonance spectrum, providing evidence that DEHP stimulates (*)OH radical formation in vivo. Furthermore, when rats were pretreated with dietary glycine, which inactivates Kupffer cells, DEHP did not increase radical signals. Moreover, similar treatments were performed in knockout mice deficient in NADPH oxidase (p47(phox) subunit). Importantly, DEHP increased oxidant production in wild-type but not in NADPH oxidase-deficient mice. These data provide evidence for the hypothesis that the molecular source of free radicals induced by peroxisome proliferators is NADPH oxidase in Kupffer cells. On the contrary, radical adduct formation was not affected in peroxisome proliferator-activated receptor alpha knockout mice. These observations represent the first direct, in vivo evidence that phthalates increase free radicals in liver before peroxisomal oxidases are induced.

Age-related change of free radical generation in liver and sex glands of rats

Many investigations have been made on age-related changes of lipid peroxidation in tissue homogenates and subcellular fractions. However, to date there are few reports on the age-related change of free radicals in living organs during aging. In our study, we investigated free radical concentration in liver and sex glands of different aged rats by using electron spin resonance (ESR) technique. A significant reduction of free radicals in liver and sex glands of old aged rats was observed when compared with those of young or middle-aged ones. The decrease of free radical generation during aging is discussed.

Effects of dietary zinc on free radical generation, lipid peroxidation, and superoxide dismutase in trained mice

The purpose of this study was to investigate the effects of dietary zinc on free radical generation, lipid peroxidation, and superoxide dismutase (SOD) in exercised mice. In the first part of the study, 48 male weanling mice were randomly divided into three groups. They were fed a zinc-deficient diet containing 1.6 mg/kg zinc or were pair-fed or fed ad libitum a zinc-adequate diet supplemented with 50 mg/kg zinc. Half of each group received an exercise training program that consisted of swimming for 60 min per day in deionized water. The diets and exercise program persisted for 6 weeks. In the second part of the study, 64 mice were fed zinc-deficient diets for 6 weeks, and then one group was fed the zinc-deficient diet for an additional 3 weeks, and the other three groups were fed diets supplemented with 5, 50, and 500 mg/kg zinc, respectively. Half of each group also received the exercise program. Both blood and liver samples were examined. Free radicals in liver were directly detected by electron spin resonance techniques and the extent of lipid peroxidation was indicated by malonic dialdehyde (MDA). Both CuZn-SOD and Mn-SOD were measured. The results showed that exercise training increased the metabolism of zinc, and zinc deficiency induced an increased free radical generation and lipid peroxidation and a decreased hepatic CuZn-SOD activity in exercised mice. Furthermore, although exercise training had no effect on the level of free radicals in zinc-adequate mice, it could increase the hepatic mitochondrial MDA formation further in zinc-deficient animals and zinc deficiency would eliminate the exercise-induced increase in SOD activities which existed in zinc-adequate mice. A total of 50 mg/kg zinc supplemented in the diet was adequate to correct the zinc-deficient status in exercised mice while 5 mg/kg zinc had a satisfactory effect on the recovery of only sedentary zinc-deficient mice. However, 500 mg/kg zinc had a harmful effect on both sedentary and exercised zinc-deficient animals.

Reactive free radical generation in vivo in heart and liver of ethanol-fed rats: correlation with radical formation in vitro.

Rats fed a high-fat ethanol-containing diet for 2 weeks were found to generate free radicals in liver and heart in vivo. The radicals are believed to be carbon-centered radicals, were detected by administering spin-trapping agents to the rats, and were characterized by electron paramagnetic resonance spectroscopy. The radicals in the liver were demonstrated to be localized in the endoplasmic reticulum. Rats fed ethanol in a low-fat diet showed significantly less free radical generation. Control animals given isocaloric diets without ethanol showed no evidence of free radicals in liver and heart. When liver microsomes prepared from rats fed the high-fat ethanol diet were incubated in a system containing ethanol, NADPH, and a spin-trapping agent, the generation of 1-hydroxyethyl radicals was observed. The latter was verified by using 13C-substituted ethanol. Microsomes from animals fed the high-fat ethanol-containing diet had higher levels of cytochrome P-450 than microsomes from rats fed the low-fat ethanol-containing diet. The results suggest that the consumption of ethanol results in the production of free radicals in rat liver and heart in vivo that appear to initiate lipid peroxidation.