• 제목/요약/키워드: Oxidative damage

검색결과 1,489건 처리시간 0.027초

마늘 추출물이 간 손상 랫드의 조직학적 변화에 미치는 효과 연구 (A Study of the Histological Effects of Garlic Extract in a Liver-damage Rat Model)

  • 이태종;민경진
    • 한국환경보건학회지
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    • 제36권4호
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    • pp.279-287
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    • 2010
  • In this study we examined the effects of water extract of garlic on carbon tetrachloride-induced liver injury, and demonstrated increased beneficial enzyme and anti-oxidant activity as well as histopathological changes (by Hematoxylin-Eosin (H&E) staining, Trichrome staining, and TEM examination), and showed that the treatment was dose-dependent and safe. A total of 42 male Sprague-Dawley rats were divided equally (n=7) into six groups. To induce hepatotoxicity in these subjects, carbon tetrachloride diluted in an equal volume of olive oil was intraperitoneally administrated at 0.5 ml/kg (0.20 g/kg/day) once a day for five days. Water extract of Korean-grown garlic was administered via a stomach sonde once a day, 5 days a week, for a total of 4 weeks. Groups received 0.35 g/kg (E1), 0.70 g/kg (E2), or 1.40 g/kg (E3), with the dose adjusted for body weight. Administration of garlic extract resulted in positive physiological effects in terms of reduced oxidative stress and toxicity, and induced functional changes in the liver. Comparing the subject groups (E1, E2, E3) administered different doses of garlic extract, the importance of morphological analysis in further studies is emphasized, because morphological changes indicating hepatotoxicity could occur, even though beneficial enzyme activities were found to be elevated.

Effects of Acute Lymphoblastic Leukemia on Ceruloplasmin Oxidase, Copper and Several Markers of Oxidative Damage, in Children

  • Mehdi, Wesen Adel;Yusof, Faridah;Mehde, Atheer Awad;Zainulabdeen, Jwan Abdulmohsin;Raus, Raha Ahmed;Abdulbari, Alaa Shawqi
    • Asian Pacific Journal of Cancer Prevention
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    • 제16권13호
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    • pp.5205-5210
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    • 2015
  • Background: Acute leukaemia is characterized by fast growth of abnormal clones of haemopoietic precursor cells inside bone marrow leading to undue accumulation in the bone marrow. Acute lymphoblastic leukemia (ALL) is the most common form of childhood cancer. Materials and Methods: The study concerned 50 children diagnosed with ALL (mean age, $8.55{\pm}2.54$) compared to 40 healthy controls (mean age, $8.00{\pm}1.85$). The Hb, serum copper, ceruloplasmin oxidase, advanced oxidation protein products (AOPPs), total antioxidant activity (TAA) and protein were measured in all groups.One proteinous component was isolated by gel filtration chromatography from the precipitate produced by polyethylene glycol. Results: Significantly higher levels of AOPP, copper and decrease in total antioxidant activity were noted in the cases. Statistical analysis also showed a significant increase (p<0.01) in the activity of serum ceruloplasmin oxidase in patients with ALL compared to normal subjects .The maximum velocity (Vmax) and Michaelis constant had values of 104.2 U/L and 11.7 mM, respectively. The ${\Delta}H^*$ values for ceruloplasmin oxidase in ALL patients were positive, confirming the reaction to be endothermic. Conclusions: The results from this study showed a significant increase in AOPP, ceruloplasmine oxidase and decrease in total antioxidant activity .These parameters may play a role in development of DNA damage in childhood patients with acute lymphoblastic leukemia (ALL).The ${\Delta}S^*$ and ${\Delta}G^*$ values were negative, these refer that the reaction of ES formation is spontaneous, but needs energy in a so-called endergonic reaction. Also the negative ${\Delta}S^*$ value of ceruloplasmin oxidase indicates that the complex [$ES^*$] is further modulated through increasing structure arrangement.

Mechanisms of Cadmium Carcinogenicity in the Gastrointestinal Tract

  • Bishak, Yaser Khaje;Payahoo, Laleh;Osatdrahimi, Alireza;Nourazarian, Alireza
    • Asian Pacific Journal of Cancer Prevention
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    • 제16권1호
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    • pp.9-21
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    • 2015
  • Cancer, a serious public health problem in worldwide, results from an excessive and uncontrolled proliferation of the body cells without obvious physiological demands of organs. The gastrointestinal tract, including the esophagus, stomach and intestine, is a unique organ system. It has the highest cancer incidence and cancer-related mortality in the body and is influenceed by both genetic and environmental factors. Among the various chemical elements recognized in the nature, some of them including zinc, iron, cobalt, and copper have essential roles in the various biochemical and physiological processes, but only at low levels and others such as cadmium, lead, mercury, arsenic, and nickel are considered as threats for human health especially with chronic exposure at high levels. Cadmium, an environment contaminant, cannot be destroyed in nature. Through impairment of vitamin D metabolism in the kidney it causes nephrotoxicity and subsequently bone metabolism impairment and fragility. The major mechanisms involved in cadmium carcinogenesis could be related to the suppression of gene expression, inhibition of DNA damage repair, inhibition of apoptosis, and induction of oxidative stress. In addition, cadmium may act through aberrant DNA methylation. Cadmium affects multiple cellular processes, including signal transduction pathways, cell proliferation, differentiation, and apoptosis. Down-regulation of methyltransferases enzymes and reduction of DNA methylation have been stated as epigenetic effects of cadmium. Furthermore, increasing intracellular free calcium ion levels induces neuronal apoptosis in addition to other deleterious influence on the stability of the genome.

The therapeutic effects of WSY-0702 on benign prostatic hyperplasia in RWPE-1

  • Oh, Hyun-A;Kwon, Eun Bi;Hwang, Yun Gyeong;Park, Soon Eung;Mok, Ji Ye;Hwang, Sung Yeoun
    • 셀메드
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    • 제7권2호
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    • pp.8.1-8.7
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    • 2017
  • Benign prostatic hyperplasia (BPH) is one of the major diseases of the urinary system in older men. WSY-0702 is the extracted from the traditional medicinal plant; Seoritae, and it has effects of anti-obesity, chronic cervical pain, and anti-oxidant. The present study aimed to investigate the therapeutic potential of WSY-0702 in the prevention and treatment of BPH. Several parameters including inflammatory mediators, hormones, and oxidative stress (OS) have been considered to play a role in the development of BPH. Prostate tissue damage and OS may lead to compensatory cellular proliferation with resulting hyperplastic growth. An in vitro study showed that proliferation inhibited the human prostate epithelial cell line RWPE-1 in a dose-dependent manner. In cell line, the cell cycle at the G2/M and G0/G1 phase and downregulated the expression of CyclineB1 (CCNB1) and CyclineD1 (CCND1). In addition, we measured the $H_2O_2$-induced OS damage using RWPE-1 cells. We examined the relative expression of protein involved in the regulation of prostate apoptosis: transforming growth factor (TGF)-${\beta}$, a negative growth factor able to induced prostate apoptosis under physiological conditions. These results suggest that WSY-0702 that can inhibit the growth of prostate epithelial cell by a mechanism that may involve arresting the cell cycle and downregulating CCNB1 and CCND1 expression. In addition, WSY-0702 exposure resulted in significant protective effects in $H_2O_2$-stressed PWPE-1 cells by reduction in TGF-${\beta}$ levels.

과산화수소수로 유도된 배양 뇌신경세포손상에 대한 왕머루 잎과 줄기 추출물의 보호효과 (Protective Effect of Vitis amurensis Stems and Leaves Extract on Hydrogen Peroxide-induced Oxidative Neuronal Cell Damage in Cultured Neurons)

  • 김주연;주현수;반주연;송경식;배기환;성연희
    • 한국약용작물학회지
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    • 제17권1호
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    • pp.68-74
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    • 2009
  • Vitis amurensis (VA; Vitaceae) has long been used in oriental herbal medicine. It has been reported that roots and seeds of VA have anti-inflammatory and antioxidant effects. In the present study, the protective effect of ethanol extract from stems and leaves of VA on hydrogen peroxide (${H_2}{O_2}$) (100 ${\mu}M$)-induced neuronal cell damage was examined in primary cultured rat cortical neurons. VA (10-100 ${\mu}g$/ml) concentration-dependently inhibited ${H_2}{O_2}$-induced apoptotic neuronal cell death measured by 3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. VA inhibited ${H_2}{O_2}$-induced elevation of intracellular $Ca^{2+}$ concentration (${[Ca^{2+}]}_i$) and generation of reactive oxygen species (ROS), which were measured by fluorescent dyes. Pretreatment of VA also prevented glutamate release into medium induced by 100 ${\mu}M$ ${H_2}{O_2}$, which was measured by HPLC. These results suggest that VA showed a neuroprotective effect on ${H_2}{O_2}$-induced neuronal cell death by interfering with ${H_2}{O_2}$-induced elevation of ${[Ca^{2+}]}_i$, glutamate release, and ROS generation. This has a significant meaning of finding a new pharmacological activity of stems and leaves of VA in the CNS.

Combination of Vitamin C and Rutin on Neuropathy and Lung Damage of Diabetes Mellitus Rats

  • Sohn, Uy-Dong;Je, Hyun-Dong;Shin, Chang-Yell;Park, Sun-Young;Yim, Sung-Hyuk;Kum, Chan;Huh, In-Hoi;Kim, Jin -Hak
    • Archives of Pharmacal Research
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    • 제25권2호
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    • pp.184-191
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    • 2002
  • We investigated the role of vitamin C or rutin on neuropathy and lung damage of diabetic mellitus(DM) rats. Norepinephrine content was significantly decreased in sciatic nerves of DM rats compared with non-DM controls but vitamin C had no effect on decreases of norepinephrine. 2,4-dinitrophenylhydrazine (DNPH) incorporation, which is biomarker of protein oxidation, was increased in sciatic nerve of DM rats as compared with normal control. However, vitamin C had no effects on increases of DNPH incorporation . We measured the content of conjugated dienes (CD) as a biomarker of lipid oxidation in sciatic nerve. CD was increased in DM as compared with normal control, Vitamin C or rutin had no effects on increases of CD. However, Rutin plus vitamin C significantly decreased the content of CD as compared with CIM rats. In lung of DM rats, DNPH incorporation or CD was increased as compared with normal control. Vitamin C or Rutin had no effects on increases of CD However, Rutin plus vitamin C significantly decreased the content of DNPH incorporation or CD in lung tissue. Vitamin C caused marked pathological changes such as the increases of parenchyma and the thickening of alveolar septa in the lung of DM. Rutin had protective effects on the pathological changes in the lung of DM rats. In conclusion, Vitamin C had no effects on oxidative parameter, such as DNPH incorporation or CD, and on the decreases of norepinephrine content in DM rats. Vitamin C caused the marked pathological changes in the lung of DM rats but rutin had protective efforts against the pathological changes.

Effect of Copper Ion on Oxygen Damage in Superoxide Dismutase-Deficient Saccharomyces Cerevisiae

  • Lee, Jeong-Ki;Kim, Ji-Myon;Kim, Su-Won;Nam, Doo-Hyun;Yong, Chul-Soon;Huh, Keun
    • Archives of Pharmacal Research
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    • 제19권3호
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    • pp.178-182
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    • 1996
  • Using superoxide dismutase (SOD)-deficient mutants of Saccharomyces cerevisiae, the oxidative stresses induced by 0.1 mM of copper ion $(Cu^{++})$ was studied. In aerobic culture condition, yeasts lacking MnSOD (mitochondrial SOD) showed more significant growth retardation than CuZnSOD (cytoplasmic SOD)-deficient yeasts. However, not so big differences in growth pattern of those mutants compared withwild type were observed under anaerobic condition. It was found that, under aerobic condition, the supplementation of 0.1 mM copper ioh:(Cu") into culture medium caused the remarkable increase of CuZnSOD but not so significant change in MnSOD. It was also observed that catalase activities appeared to be relatively high in the presence of copper ion in spite of the remarkable reduction of glutathion peroxidase in CuZnSOD-deficient yeasts, but the slight increments of catalase and glutathion peroxidase were detected in MnSOD-deficient strains. It implies that the lack of cytoplasmic SOD could be compensated mainly by catalase. However, these phenomena resulted in the significantincrease of cellular lipid peroxides content in CuZnSOD-deficient yeasts and the slight increment of lipid peroxides in MNSOD-deficient cells. In anaerobic cultivation supplementing copper ion, the cellular enzyme activities of catalase and glutathion peroxidase in SOD-deficient yeasts were slightly increased without any significant changes of lipid peroxides in cell membrane. It suggests that a little amount of free radicals generated by copper ion under anaerobic condition could be sufficiently overcome by catalase as well as glutathion peroxidase.dase.

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Nitric oxide modulates antioxidant defense and the methylglyoxal detoxification system and reduces salinity-induced damage of wheat seedlings

  • Hasanuzzaman, Mirza;Hossain, Mohammad Anwar;Fujita, Masayuki
    • Plant Biotechnology Reports
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    • 제5권4호
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    • pp.353-365
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    • 2011
  • The present study investigates the possible regulatory role of exogenous nitric oxide (NO) in antioxidant defense and methylglyoxal (MG) detoxification systems of wheat seedlings exposed to salt stress (150 and 300 mM NaCl, 4 days). Seedlings were pre-treated for 24 h with 1 mM sodium nitroprusside, a NO donor, and then subjected to salt stress. The ascorbate (AsA) content decreased significantly with increased salt stress. The amount of reduced glutathione (GSH) and glutathione disulfide (GSSG) and the GSH/GSSG ratio increased with an increase in the level of salt stress. The glutathione S-transferase (GST) activity increased significantly with severe salt stress (300 mM). The ascorbate peroxidase (APX), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), catalase (CAT) and glutathione peroxidase (GPX) activities did not show significant changes in response to salt stress. The glutathione reductase (GR), glyoxalase I (Gly I), and glyoxalase II (Gly II) activities decreased upon the imposition of salt stress, especially at 300 mM NaCl, with a concomitant increase in the $H_2O_2$ and lipid peroxidation levels. Exogenous NO pretreatment of the seedlings had little influence on the nonenzymatic and enzymatic components compared to the seedlings of the untreated control. Further investigation revealed that NO pre-treatment had a synergistic effect; that is, the pre-treatment increased the AsA and GSH content and the GSH/GSSG ratio, as well as the activities of MDHAR, DHAR, GR, GST, GPX, Gly I, and Gly II in most of the seedlings subjected to salt stress. These results suggest that the exogenous application of NO rendered the plants more tolerant to salinity-induced oxidative damage by enhancing their antioxidant defense and MG detoxification systems.

Inhibition of Apoptosis by Elaeocarpus sylvestris in Mice Following Whole-body Exposure to Ionizing Radiation: Implications for Radioprotectors

  • Park, Eun-Jin;Lee, Nam-Ho;Ahn, Gin-Nae;Baik, Jong-Seok;Lee, Je-Hee;Hwang, Kyu-Kye;Park, Jae-Woo;Jee, Young-Heun
    • Food Science and Biotechnology
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    • 제17권4호
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    • pp.718-722
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    • 2008
  • Elaeocarpus sylvestris var. ellipticus (E.S.), which contains 1, 2, 3, 4, 6-penta-O-galloyl-beta-D-glucose (PGG), is reported to have the ability to scavenge oxygen radicals, thereby protecting rat neuronal cells from oxidative damage. The potential of an E.S. extract, which contains a rich PGG, to protect radiosensitive lymphocytes and intestinal crypt cells from radiation injury induced by a single whole-body irradiation (WBI) in vivo was investigated. Our results demonstrated that in immune cells, E.S. treatment decreased the percent of tail DNA, a parameter of DNA damage, compared with levels in untreated, irradiated controls. Furthermore, apoptosis was significantly decreased in lymphocytes and intestinal crypt cells of E.S.-treated mice compared with irradiated controls. These results suggest that the E.S. extract can strengthen the radioresistance of radiosensitive lymphocytes and crypt cells by preventing apoptosis. Therefore, it was concluded that E.S. extract has the radioprotective effects in vivo through an inhibition of apoptosis.

Inactivation of Sirtuin2 protects mice from acetaminophen-induced liver injury: possible involvement of ER stress and S6K1 activation

  • Lee, Da Hyun;Lee, Buhyun;Park, Jeong Su;Lee, Yu Seol;Kim, Jin Hee;Cho, Yejin;Jo, Yoonjung;Kim, Hyun-Seok;Lee, Yong-ho;Nam, Ki Taek;Bae, Soo Han
    • BMB Reports
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    • 제52권3호
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    • pp.190-195
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    • 2019
  • Acetaminophen (APAP) overdose can cause hepatotoxicity by inducing mitochondrial damage and subsequent necrosis in hepatocytes. Sirtuin2 (Sirt2) is an $NAD^+$-dependent deacetylase that regulates several biological processes, including hepatic gluconeogenesis, as well as inflammatory pathways. We show that APAP decreases the expression of Sirt2. Moreover, the ablation of Sirt2 attenuates APAP-induced liver injuries, such as oxidative stress and mitochondrial damage in hepatocytes. We found that Sirt2 deficiency alleviates the APAP-mediated endoplasmic reticulum (ER) stress and phosphorylation of the p70 ribosomal S6 kinase 1 (S6K1). Moreover, Sirt2 interacts with and deacetylates S6K1, followed by S6K1 phosphorylation induction. This study elucidates the molecular mechanisms underlying the protective role of Sirt2 inactivation in APAP-induced liver injuries.