Adriamycin is a commonly used chemotherapeutic agent for cancer, including acute leukemia, lymphoma, and a number of solid human tumors. However, recent studies have recognized severe cardiotoxicity after an acute dose, which are likely the result of generation of free radicals and lipid peroxidation. Therefore, the clinical uses of adriamycin have been limited. Melatonin, the pineal gland hormone known for its ability to modulate circardian rhythm, has recently been studied in its several functions, including cancer growth inhibition, stimulating the immune system, and acting as an antioxidant and radical scavenging effects. In the present study, we evaluated the effect of melatonin administration on adriamycin-induced cardiotoxicity in rat. Heart slices were prepared using a Stadie-Riggs microtome for the measurement of malondialdehyde (MDA) content used as an index of lipid peroxidation and lactate dehydrogenase (LDH) release as an indicator of lethal cell injury. Serious adriamycin-induced lethality was observed in rat by a single intraperitoneal injection in a dose-dependent manner. A single injection of adriamycin (25 mg/kg, i.p.) induced a lethality rate of 86%, with melatonin (10 mg/kg s.c. for 6 days) treatment reducing the adriamycin-induced lethality rate to 20%. The severe body weight loss caused by adriamycin was also significantly attenuated by melatonin treatment. Treatment of melatonin marked reduced adriamycin-induced the levels of MDA formation and LDH release. A cell damage indicated by the loss of myofibrils, swelling of the mitochondria as well as cytoplasmic vacuolization was seen in adriamycin-treated group. Melatonin attenuated the adriamycin-induced structural alterations. These data provide evidence that melatonin prevents adriamycin-induced cardiotoxicity and might serve as a combination with adriamycin to limit free radical-mediated cardiotoxicity.
Vanadium has been known as environmental polluants resulted from the burning of fossil fuels in nature. It led to toxic responses by prooxidant activity, inducing free radicals and the accumulation in the tissues. Recently, there has been growing interest in an essential nutritional requirement of vandium and especially the treatment of diabetes. But because of its strong toxicity, thease chemicals have narrow safety margin. In order to reduce metal toxicity, and increase absorption and biological activities, metal ions such as selenium and chromium were uptaken in yeast cells. In this study, Vanadium yeast was prepared by uptaking vanadate in yeast cells. Vanadate induced hematological and biochemical changes in the experimental rat blood were inhibited by the treatments of vanadium yeast. Lipid peroxidation and catalase activity were significantly increased in kidney and liver after a single intraperitoneal injection of vanadate to rats. However, these observations were apparently reduced in the vanadium yeast treated group. Vanadium amount in blood, kidney and liver after a single intraperitoneal injection of vanadium yeast was significantly reduced than that of vanadate treated group. In conclusion, vanadium yeast uptaken vanadate in yeast cells could reduce toxic effects of vanadate.
TO evaluate an effect of cyclohexane treatment on the degree of liver damage, rats were induced liver damage with 10 or 17 times $CCl_4$ injection (0.1 m1/100 g body wt., 50% $CCl_4$ dis-solved in olive oil) at intervals of every other day. Cyclohexane (1.56 g/kg body wt., i.p.) was administrated to the animals at 48 hours after the last pretreatment of $CCl_4$ . Rats were sacrificed at 4 hours after injection of cyclohexane. On the basis of histopathological findings, liver weight/body weight (LW/ BW, %), activities of serum alanine aminotransferase (ALT), xanthine oxidase (XO) and akaline phosphatase (ALP), and contents of liver protein and manlondialdehyde (MDA), $CCl_4$ -pretreatment induced liver damage. And $CCl_4$ 17 times treated group showed more severe liver damage than $CCl_4$ 10 times treated group. Administration of one dose of cyclohexane to $CCl_4$ 10 times treated animals resulted in the enhanced liver damage; liver necrosis with proliferation of fibroblast and bile duct abnormality, and increase in hepatic MDA content and the activities of serum ALP and ALT, But the enhanced liver damage was not found in $CCl_4$ 17 times treated animals. Serum cyclohexanone concentrations at 4 or 8 hours after injection of cyclohexane were higher in all liver damaged groups than normal group and were somewhat higher In $CCl_4$ 17 times treated animals than $CCl_4$ 10 times treated ones. Among the oxygen free radical metabolizing enzymes, hepatic cytochrome P45O dependent aniline hydroxylase (CYPdAH) activity in cyclohexane metabolizing enzyme system was meaningfully increased by the injection of cyclohexane to the liver damaged rats, with increased Vmax and high affinity to aniline. LW/BW (%) and activities of serum XO and ALT were more significantly increased in liver damaged groups than normal group by administration of cyclohexanone. In conclusion, it is assumed that an enhancement of liver damage by injection of one dose of cyclohexane to liver damaged animals might be caused by oxygen free radicals and cyclohexanone.
Sharma, Manju;Anwer, Tarique;Pillai, K K;Haque, Syed Ehtaishamul;Najmi, A K;Sultana, Yasmin
Advances in Traditional Medicine
/
v.8
no.2
/
pp.146-153
/
2008
The present study is aimed at finding the influence of silymarin (a flavonoid) (25 mg/kg & 50 mg/kg) in streptozotocin (STZ)-induced diabetic rats. Type 2 diabetes was induced by single intraperitoneal injection of STZ (100 mg/kg) to 3 days old rat pups. Silymarin was administered for 15 days after the animals were confirmed diabetic (75 days after STZ injection). Blood glucose, glycosylated hemoglobin ($HbA_{1c}$), lipid peroxides (LPO) levels and reduced glutathione (GSH) contents in pancreas and liver were estimated following the established procedures. Biochemical observations were further substantiated with histological examination of pancreas. Blood glucose and $HbA_{1c}$ levels, which were elevated by STZ, were lowered to physiological levels by the administration of silymarin. The levels of LPO were significantly increased in STZ-induced diabetic rats. Silymarin reduced the LPO levels in both pancreas and liver. GSH contents which were reduced significantly in pancreas and liver of STZ-induced diabetic rats were brought back to near normal levels by silymarin treatment. Multifocal necrotic and degenerative changes of pancreas in STZ-diabetic rats were minimized to near normal morphology by administration of silymarin as evident by histopathological examination. Silymarin showed a dose dependent protective effect on STZ-induced $\beta$-cell damage. It could be attributed to the antioxidative and free radicals scavenging properties of the flavonoid. Thus, it may be considered as a natural antioxidant with potential therapeutic application in the treatment of type 2 diabetes.
Background: Based on the known immunoregulatory functions of moxifloxacin on phagocytes, the therapeutic effect of moxifloxacin on oleic acid (OA)-induced acute lung injury (ALI) was investigated. Methods: Moxifloxacin (10 mg/kg) was given to male Sprague-Dawley rats that had been given oleic acid (OA, $30{\mu}L$) intravenously. Five hours after OA injection, parameters demonstrating ALI were assessed to measure the effects of moxifloxacin on acute lung injury. Results: The pathological findings of OA-induced ALI's was diminished by moxifloxacin. Through ultrastructural and $CeCl_3$ EM histochemistry, moxifloxacin was confirmed to be effective in decreasing oxidative stress in the lung as well. Indices of ALI, such as lung weight/body weight ratio, protein content in bronchoalveolar lavage fluid, and lung myeloperoxidase were decreased by moxifloxacin. In diaminobenzidine immunohistochemistry, fluorescent immunohistochemistry, and Western blotting of the lung, moxifloxacin had decreased the enhanced expression of secretory phospholipase $A_2$ ($sPLA_2$) by OA. Conclusion: We concluded that moxifloxacin was effective in lessening acute inflammatory pulmonary edema caused by OA, by inhibiting the neutrophilic respiratory burst, which was initiated by the activation of $sPLA_2$.
Objectives : This study was designed to compare the effects of acanthopanax stem bark (ASB) and acanthopanax root bark (ARB) on the monosodium iodoacetate (MIA)-induced osteoarthritis rats. Methods : The antioxidant activities were evaluated through radical scavenging assays using 2,2'-azino-bis (3-ethylbenzothiazoline-6-sulphonic acid) (ABTS) radicals and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals. Also, we examined total poly phenol and flavonoids contents. Osteoarthritis was caused by injection MIA($50{\mu}{\ell}$ with $80mg/m{\ell}$) into the knee joint cavity of rats. Rats were divided by 4 groups (normal group, control group, ASB treated group, ARB treated group, each n=6). The changes in the levels of reactive oxygen species (ROS), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum were analyzed after experiment. Also, the anti-oxidant, inflammatory protein levels were investigated western blot analysis. Knee joint tissue, histopathological observation hematoxylin & eosin staining and safranin-O staining were measured. Results : In the present study, ARB treated group showed superior inhibitory effects on the inflammatory parameters than the ASB treated group. ARB aqueous extract was effective in antioxidant measurements. The administration of ARB showed a significant reduction of changes in relative hind paw weight distribution. Morever, it decreased ROS, ALT and AST levels in serum, compared with those of the control rats. The ARB administration inhibited the biomarkers of inflammatory in tissues. Conclusions : ASB aqueous extract and ARB aqueous extract have a great effect on osteoarthritis, and ARB aqueous extract has excellent effect on osteoarthritis through antioxidant and anti-inflammation.
Kim, Chung-Hui;Han, Jin;Kim, Na-Ri;Park, Ju-Hee;Yang, Young-Churl;Kim, Eui-Yong
The Korean Journal of Physiology and Pharmacology
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v.5
no.3
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pp.223-230
/
2001
Melatonin, a pineal gland hormone, is believed to act as an antioxidant via the stimulation of radical detoxifying enzymes and scavenging of free radicals. In this study, effects of in vitro and in vivo treatments of melatonin on the cisplatin-induced lipid peroxidation, LDH release and plasma creatinine were determined in rabbit renal cortical cells. The level of malondialdehyde (MDA) was assayed as an index of lipid peroxidation and the level of LDH release as an indicator of cellular damage. In in vitro studies, cisplatin increased the levels of MDA and LDH release in a concentration-and time-dependent manner. Melatonin inhibited the cisplatin-induced lipid peroxidation and LDH release in a concentration-dependent manner. The minimal effective concentration of melatonin that significantly reduced the $300\;{\mu}M$ cisplatin-induced lipid peroxidation and LDH release was 1 mM. In in vivo studies, the levels of lipid peroxidation and LDH release in renal cortical cells increased significantly 24 or 48 hours after a single injection of cisplatin (6 mg/kg). When the cisplatin-injected rabbits were pretreated with 10 mg/kg of melatonin, a significant reduction in both lipid peroxidation and LDH release was observed. The plasma creatinine level increased from $0.87{\pm}0.07$ mg/dl in control to $6.33{\pm}0.54$ mg/dl in cisplatin-injected rabbits (P<0.05). Melatonin partially prevented the increase in serum creatinine level $(1.98{\pm}0.11\;mg/dl)$ by cisplatin (P<0.05). In the proximal tubules from cisplatin-treated group, tubular cells had microvilli of variable heights. Necrotic debris was seen in tubular lumens. In most of cells, the mitochondria and lysosomes were increased in frequency. The endocytic vacuoles were not prominent and distribution of the brush border was irregular and shortened. These cisplatin-induced morphological changes were moderate in the melatonin-pretreated group. These results suggest that the toxicity of cisplatin is associated with the generation of reactive oxygen free radicals and that melatonin is a powerful antioxidant, which prevents some of the adverse effects of cisplatin.
Park, Jong-Sang;Kang, Byung-Mu;Yeum, Jung-Kuk;Ha, Jong-Yul;Chung, Sung-Sik
Journal of ILASS-Korea
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v.10
no.2
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pp.1-9
/
2005
An experimental study was carried out to obtain the fundamental data about the effects of radical ignition on premixture combustion. A CVC(constant volume combustor) divided into the sub-chamber and the main chamber was used. Numerous narrow passage holes are arranged between the main chamber and the sub-chamber. The products including radicals generated by spark ignition in tile sub-chamber derives the simultaneous multi-point ignition in the main chamber. We have examined the effects of the sub-chamber volume, the diameter and number of passage holes, and the equivalence $ratio({\Phi})$ on the combustion characteristics by means of burning pressure measurement and flame visualization. In a CVC, the overall burning time including the ignition delay became very short and the maximum burning pressure was slightly increased by the radical ignition(RI) method in comparison with those by the conventional spark ignition(SI) method. Combustible lean limit by RI method is extended by ${\Phi}=0.25$ compared with that by SI method. Also, In cases of charging the number and the diameter for the fixed total cross section of the passage holes, combustion period increased significantly at a sub-chamber with a single hole, but those of the other conditions had almost a similar tendency in the sub-chamber with 4 or more holes. regardless of equivalence ratio. Therefore, it was Proved that a critical cross section exists with the number of passage holes.
Proceedings of the Korean Vacuum Society Conference
/
2010.08a
/
pp.128-128
/
2010
In this study, we investigated the evolution and reduction of the surface roughness during the high-speed chemical dry thinning process of Si wafers. The direct injection of NO gas into the reactor during the supply of F radicals from NF3 remote plasmas was very effective in increasing the Si thinning rate, due to the NO-induced enhancement of the surface reaction, but resulted in the significant roughening of the thinned Si surface. However, the direct addition of Ar and N2 gas, together with NO gas, decreased the root mean square (RMS) surface roughness of the thinned Si wafer significantly. The process regime for the increasing of the thinning rate and concomitant reduction of the surface roughness was extended at higher Ar gas flow rates. In this way, Si wafer thinning rate as high as $20\;{\mu}m/min$ and very smooth surface roughness was obtained and the mechanical damage of silicon wafer was effectively removed. We also measured die fracture strength of thinned Si wafer in order to understand the effect of chemical dry thinning on removal of mechanical damage generated during mechanical grinding. The die fracture strength of the thinned Si wafers was measured using 3-point bending test and compared. The results indicated that chemical dry thinning with reduced surface roughness and removal of mechanical damage increased the die fracture strength of the thinned Si wafer.
Proceedings of the Korean Vacuum Society Conference
/
2010.02a
/
pp.392-392
/
2010
In this study, high-speed chemical dry thinning process of Si wafer and evolution of surface roughness were investigated. Direct injection of NO gas into the reactor during the supply of F radicals from $NF_3$ remote plasmas was very effective in increasing the Si thinning rate due to the NO-induced enhancement of surface reaction but thinned Si surface became roughened significantly. Addition of Ar gas, together with NO gas, decreased root mean square (RMS) surface roughness of thinned Si wafer significantly. The process regime for the thinning rate enhancement with reduced surface roughness was extended at higher Ar gas flow rate. Si wafer thinning rate as high as $22.8\;{\mu}m/min$ and root-mean-squared (RMS) surface roughness as small as 0.75 nm could be obtained. It is expected that high-speed chemical dry thinning process has possibility of application to ultra-thin Si wafer thinning with no mechanical damage.
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