• Annals of Clinical Neurophysiology
• /
• v.8 no.1
• /
• pp.63-70
• /
• 2006

Background: Testosterone is reported to have neuroprotective effect in various neurological diseases. Recently, the mechanism involved in nitric oxide (NO)-mediated motor neuron death is under extensive investigation. The Cu/Zn-superoxide dismutase (SOD1) mutations has been implicated in selective motor neuron death of amyotrophic lateral sclerosis (ALS) and it is said to play an important role in NO-mediated motor neuron death. However, neuroprotective effect of testosterone on motor neuron exposed to NO has rarely been studied. Methods: Motor neuron-neuroblastoma hybrid cells expressing wild-type or mutant (G93A or A4V) SOD gene were treated with $200{\mu}M$ S-nitrosoglutathione. After 24 hr, cell viability was measured by MTT assay. To see the neuroprotective effect of testosterone, pretreatment with 1 nM testosterone was done 1 hr before S-nitroglutathione treatment. To study the mechanism of protective effect, $20{\mu}M$ flutamide (androgen receptor antagonist) was also pretreated with testosterone 1 hr before S-nitroglutathione treatment. Results: S-nitrosoglutathione showed significant neurotoxic effect in all three cell lines. Percentage of cell death was somewhat different in each cell line. 1 nM testosterone showed neuroprotective effect in G93A and wild-type cell line. In A4V cell line, testosterone did not showed neuroprotective effect. The neuroprotective effect of testosterone was reversed by $20{\mu}M$ flutamide. Conclusions: These results indicate that testosterone induces neuroprotection in NO-mediated motor neuron death directly through the androgen receptor. This neuroprotective effect of testosterone varies according to the types of SOD1 gene mutation. These data suggest that testosterone may be of therapeutic value against ALS.

• Journal of Periodontal and Implant Science
• /
• v.36 no.1
• /
• pp.97-112
• /
• 2006

유리 라디칼과 활성 산소종, 산화방지제 간의 불균형이 염증성 구강내 질환의 발생과 진행에 있어 중요한 역할을 한다는 주장이 제기되었고 최근에는 만성 염증성 치주질환에서도 산화에 의한 소실이 관찰되었다. 다양한 내적인 항산화 방어 기전 중 superoxide dismutase 가 $O_2$를 $H_2O_2$로 효과적으로 전환시킴으로써 활성산소종에 대한 일차적인 방어를 맡고 있다. 현재까지 인간에서 발견된 superoxide dismutase 는 cytoplasmic copper-zinc SOD와 mitochondrial manganase SOD, extracellular SOD의 3가지 아형이다. 이번 연구는 만성 치주질환을 가전 환자의 치주조직에서 효소 항산화제인 SOD의 발현정도를 알아봄으로써 질환조직 내의 산화자극 정도를 평가해 보고자하였다. 전남대학교 치주과에 내원한 33명의 만성 치주질환자와 20명 의 임상적으로 건강한 대상으로부터 조직을 얻어 Cu/Zn-SOD와 Mn-SOD, EC-SOD를 이용한 면역조직화학 염색을 시행하였다. 임상적 소견과 조직학적 소견이 일치하지 않아 조직학적 소견을 기준으로 건강한 조직, 경도, 중등도, 중도 치주질환 조직으로 그룹을 나누고 완전한 상피와 결합조직을 가진 27개의 표본에 대한 분석을 시행하였다. 치주질환 조직에서 건강한 조직에 비해 Cu/Zn-SOD가 상피의 기저층과 상피에 근접한 결합조직에서 발현되고 Mn-SOD는 염증이 증가함에 따라 크게 상피의 과립증과 각화층, 그리고 상피에 근접한 결합조직에서 발현됨으로써 활성산소종이 치주조직 파괴에 관여한다는 것을 알 수 있었다. 세 아형 모두 혈관주위에서 발현되었고 특히 EC-SOD는 작은 모세혈관주위에서만 발현되었으나 염증에 의해 혈관벽이 두꺼워지고 혈관 수가 증가한 곳에서 뚜렷하게 염색되었다. 이번 연구는 염증성 치주조직내 증가된 SOD의 활성이 치주질환자의 산화자극 정도와 관련되어 있음을 시사하였다.

• Plant Resources
• /
• v.7 no.3
• /
• pp.163-169
• /
• 2004

To investigate the defense mechanism against the abiotic stress, a cDNA clone encoding a CuZn superoxide dismutase (CuZnSOD) protein was isolated from a cDNA library prepared from tabroot mRNAs of Codonopsis lanceolata. The eDNA, designated ClSODCc, is 799 nucleotides long and has an open reading frame of 459 bp with a deduced amino acid sequence of 152 residues. The deduced amino acid sequence of ClSODCc matched to the previously reported CuZnSODs. Consensus amino acid residues (His-45, -47, -62, -70, -79, -119 and Asp-82) were involved in Cu-, Cu/Zn-, and Zn- binding ligands. The deduced amino acid sequence of ClSODCc showed high homologies (82％-86％) regardless of species. Expression of ClSODCc by oxidative stress was increased up to 1 h after treatment and declined gradually. Much earlier and stronger expression of ClSODCc was observed in the cold stress treatment.

• Proceedings of the Zoological Society Korea Conference
• /
• 1995.10b
• /
• pp.316.2-316
• /
• 1995

No Abstract, See Full Text

• Asian-Australasian Journal of Animal Sciences
• /
• v.23 no.8
• /
• pp.1066-1072
• /
• 2010

In this study, the effects of replacing inorganic copper, zinc and manganese with different levels of organic complexes of the same trace minerals on the lipid peroxidation and antioxidant defense systems in broilers were investigated. Two-hundred Ross-308 one-day-old broiler chickens were placed on controlled diets until 42 d of age. The experimental animals were divided into four groups comprising three experimental groups and one control group, each consisting of 50 chickens. All groups were also divided into five subgroups each containing 10 broiler chicks. The mineral content of the control group diet was controlled using a standard inorganic mineral premix with supplement levels and sources of trace minerals typical of commercial broiler diets according to the National Research Council (NRC) (containing 8 mg Cu as $CuSO_4$, 40 mg Zn as $ZnSO_4$, and 60 mg Mn as MnO, per kg). In the experimental diets, mineral premix was also comprised of inorganic formulations, except for those of Cu, Zn and Mn. Organically-complexed Cu, Zn, and Mn were separately added to the basal diet at 1/3 (L1), 2/3 (L2) and 3/3 (L3) levels with respect to the NRC recommendation, as Bioplex $Cu^{TM}$, Bioplex $Zn^{TM}$, Bioplex $Mn^{TM}$. At the end of the trial, the plasma Zn level significantly increased when the plasma Cu level significantly decreased (p<0.05) in chickens fed at 2/3 and 3/3 levels of organically complexed minerals. The liver trace mineral concentrations were significantly higher in chickens fed inorganic trace minerals in comparison to those fed organically-complexed minerals. The plasma malondialdehyde (MDA) level of experimental chickens was decreased in groups receiving levels of organic Cu, Zn and Mn in comparison to those fed inorganic forms (p<0.01). The erythrocyte superoxide dismutase (SOD) activity was higher in all groups receiving the organic mineral supplements in comparison to those fed inorganic forms (p<0.01). No differences were observed on either the erythrocyte catalase (CAT) activity or the plasma ceruloplasmin (Cp) levels, and the liver MDA levels and liver CAT and SOD activities in any of the groups that received the organic supplements of Cu, Zn, and Mn. It was concluded that supplementation of lower levels of organically-complexed copper, zinc, and manganese instead of their inorganic forms in diets had no negative effects on the antioxidant defense system in broilers.

• Tuberculosis and Respiratory Diseases
• /
• v.40 no.2
• /
• pp.104-111
• /
• 1993

Background: Gram-negative bacterial endotoxin induced septicemia is known to be a leading cause in the development of adult respiratory distress syndrome(ARDS). The mechanism of endotoxin induced lung injury is mainly due to the activated neutrophils which injure the capillary endothelial cells by releasing oxidant radical and resulted in pulmonary edema. We studied the change of antioxidant enzyme in the case of large or small, intermittant dose of endotoxin infused rat lungs. Methods: Endotoxin was given to the rat through the peritoneal cavity in the dose of 7 mg/kg body weight in the large dose group and 1 mg/kg for 10 days in the small dose group. Bronchoalveolar lavage (BAL) was done and rats were killed at 6, 12, 24 hours after single endotoxin injection in the large dose group and 3, 7, 10 days after daily endotoxin injection for 10 days in the small dose group. The lungs were perfused with normal saline through the pulmonary artery to remove the blood and were homogenized in 5 volume of 50 mM potassium phosphate buffer containing 0.1 mM EDTA. After centrifuging at 100,000 g for 60 minute, the supernatent was removed and stored at $-70^{\circ}C$ until measuring for superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px) and protein. Results: We observed the following results. 1) The lung wet/dry weight ratio and albumin concentration in the BAL fluids were increased to peak at 12 hours and neutrophil number in the BAL fluids were peak at 6 hours after endotoxin injection in the large dose group. 2) Cu, Zn SOD (IU/mg protein) was significantly decreased after 6, 12 hours after endotoxin injection in the large dose group. 3) There were no singnificant change in the level of Mn SOD, catalase, GSH-Px after endotoxin injection in both groups. Conclusion: Endotoxin in the large dose group produced the acute pulmonary edema and decreased the Cu, Zn SOD in the lung tissue after injecting endotoxin at 6 and 12 hours. These phenomenon may be due to the cell membrane damage by endotoxin. Further research would be necessary whther giving SOD by intratracheal route or method to increase the synthesis of SOD may lessen the acute lung injury by endotoxin.

• Journal of Preventive Medicine and Public Health
• /
• v.23 no.4 s.32
• /
• pp.371-390
• /
• 1990

Production of free radicals of superoxide anion in tissues by cadmium, activities of superoxide dismutase and catalase to protect tissue damages caused by the free radicals and ATPase that plays an important role in energy metabolism at cellular level were investigated. Experiments in vivo were conducted with liver, kidney and testicle tissue homogenates of rats adding $0.05{\sim}0.50mM$ cadmium chloride, and in vivo experiments administering single dose of 5 mg of cadmium/kg of body weight in 0.1% cadmium chloride solution intraperitoneally 48 hours prior to evisceration. Production of superoxide radicals in liver and testicle increased with addition of cadmium in vitro, but not in kidney. In vivo experiments, however, superoxide radicals slightly increased in liver and kidney but not in testicle. Superoxide dismutase (Cu, Zn-SOD and Mn-SOD), catalase and ATPase (total, $Mg^{++}-\;&\;Na^+,\;K^+-$) activity decreased in the presence of cadimium in dose dependent manner. Reduction of these enzyme activities varied not only with dosage of cadmium but also with type of tissue and between in vitro and in vivo experiment.

• Proceedings of the KSAR Conference
• /
• 2003.06a
• /
• pp.47-47
• /
• 2003

The present study was conducted to determine the expression of the antioxidant enzyme(CuZn-SOD, Mn-SOD and GPX and apoptosis gene(caspase-3) for in vitro culture in in vitro maturation and in vitro fertilization(IVM/IVF) embryos in porcine. Porcine embryos derived from IVM/IVF were cultured in NCSU23 medium under 5% $CO_2$ in air at 38.5$^{\circ}C$. The patterns of gene expression for several antioxidant enzyme and apoptosis genes during preimplantion porcine embryo development were examined by the modified semi-quantitative single cell reverse transcriptase- polymerase chain reaction (RT-PCR). Preimplantation porcine embryos produced by IVM/IVF have expressed mRNAs for CuZn-SOD and GPX, whereas transcripts for Mn-SOD have not detected at any developmental stages. Expression of caspase-3 mRNA was detected at 2 cell, 8 cell, 16 cell and morula stages. The fas ligand transcripts were detected in porcine blastocyst. These results suggest that various antioxidant enzymes and apoptosis genes play crucial roles in in vitro culture of porcine IVM/IVF embryos.

• Molecules and Cells
• /
• v.20 no.3
• /
• pp.401-408
• /
• 2005

Reactive oxygen species (ROS) contribute to the development of various human diseases. Cu,Zn-superoxide dismutase (SOD) is one of the major means by which cells counteract the deleterious effects of ROS. SOD activity is dependent upon bound copper ions supplied by its partner metallochaperone protein, copper chaperone for SOD (CCS). In the present study, we investigated the protective effects of PEP-1-CCS against neuronal cell death and ischemic insults. When PEP-1-CCS was added to the culture medium of neuronal cells, it rapidly entered the cells and protected them against paraquat-induced cell death. Moreover, transduced PEP-1-CCS markedly increased endogenous SOD activity in the cells. Immunohistochemical analysis revealed that it prevented neuronal cell death in the hippocampus in response to transient forebrain ischemia. These results suggest that CCS is essential to activate SOD, and that transduction of PEP-1-CCS provides a potential strategy for therapeutic delivery in various human diseases including stroke related to SOD or ROS.

• Journal of Aquaculture
• /
• v.18 no.3
• /
• pp.173-179
• /
• 2005

Superoxide dismutase (SOD), an antioxidant enzyme catalyzing the first step for scavenging the reactive oxygen species is important as an early warning indicator to address various biological stresses. For this reason, the monitoring the expressed pattern of SOD gene in fish organs is one of important biomarkers to assess the aquatic pollution caused by many toxic chemicals. Based on the Northern blot hybridization, semi-quantitative and/or realtime RT-PCRs, the alteration of SOD gene transcripts in shark liver was examined during the experimental acute exposures to cadmium. The expression of SOD at mRNA level was up-regulated both by injection (0, 0.5, 1 or 2 mg $CdCl_2/kg$ body weight for 48 hours) and by immersion (0 or $5{\mu}M$ Cd for 0, 1, 4 and 7 days) treatments of cadmium. The transcriptional stimulation of shark SOD gene by cadmium exposure was dependent upon doses and durations: there was a trend toward more increase in higher dose and longer durations of exposure. The hepatic SOD mRNA levels showed also a general agreement with the tissue cadmium concentrations accumulated in immersion exposure. This result may provide useful strategy to develop a fine molecular biomarker at mRNA level for detecting aquatic pollution caused by toxic metals.