Redox imbalance

Berg, Daniela; Youdim, Moussa B. H.; Riederer, Peter

doi:10.1007/s00441-004-0976-5

Cited by 190 publications

(91 citation statements)

References 142 publications

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“…These species may attack soluble cell compounds as well as membranes, eventually leading to the impairment of cell functioning and cytolysis [21,22]. But peroxidative damages induced in the cell are encountered by elaborate defense mechanisms, including enzymic and nonenzymic antioxidants.…”

Section: Discussionmentioning

confidence: 99%

Influence of Selenium on Hepatic Mitochondrial Antioxidant Capacity in Ducklings Intoxicated with Aflatoxin B1

Shi

Guo

Liao

et al. 2011

Biol Trace Elem Res

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The aim of the study was to investigate the effect of selenium on hepatic mitochondrial antioxidant capacity in ducklings administrated with aflatoxin B(1) (AFB(1)). Ninety 7-day-old ducklings were randomly divided into three groups (groups I-III). Group I was used as a blank control. Group II was administered with AFB(1) (0.1 mg/kg body weight). Group III was administered with AFB(1) (0.1 mg/kg body weight) plus selenium (sodium selenite, 1 mg/kg body weight). All treatments were given once daily for 21 days. The results showed that the activities of mitochondrial superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione reductase (GR) in group II ducklings significantly decreased when compared with group I (P < 0.01). Furthermore, the content of hepatic mitochondrial malondialdehyde (MDA) significantly increased (P < 0.01). However, the activities of hepatic mitochondrial SOD, CAT, GSH-Px, and GR in group III ducklings significantly increased when compared with group II (P < 0.05). In addition, the content of hepatic mitochondrial MDA significantly decreased (P < 0.01). These results revealed that AFB(1) significantly induced hepatic mitochondrial antioxidant dysfunction. However, sodium selenite could significantly ameliorate the negative effect induced by AFB(1).

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Section: Discussionmentioning

confidence: 99%

Influence of Selenium on Hepatic Mitochondrial Antioxidant Capacity in Ducklings Intoxicated with Aflatoxin B1

Shi

Guo

Liao

et al. 2011

Biol Trace Elem Res

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“…These species may attack soluble cell compounds as well as membranes, eventually leading to the impairment of cell functioning and cytolysis [25]. But peroxidative damages induced in the cell are encountered by elaborate defense mechanisms, including enzymic and nonenzymic antioxidants [26].…”

Section: Discussionmentioning

confidence: 99%

Protection of Selenium on Hepatic Mitochondrial Respiratory Control Ratio and Respiratory Chain Complex Activities in Ducklings Intoxicated with Aflatoxin B1

Shi

Guo

Liao

et al. 2011

Biol Trace Elem Res

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To investigate the protection of selenium on hepatic mitochondrial functions, 90 7-day-old ducklings were randomly divided into three groups (groups I-III). Group I was used as a blank control. Group II was administered with aflatoxin B(1) (0.1 mg/kg body weight). Group III was administered with aflatoxin B(1) (0.1 mg/kg body weight) plus selenium (sodium selenite, 1 mg/kg body weight). All treatments were given once daily for 21 days. The results showed that the activities of hepatic mitochondrial complexes I-IV in group II ducklings significantly decreased when compared with group I (P < 0.01). Furthermore, the activities of hepatic mitochondrial complexes I-IV in group III significantly increased when compared with group II (P < 0.05). The hepatic mitochondrial respiratory control ratio (RCR) in group II ducklings significantly decreased when compared with group I (P < 0.01). In addition, the hepatic mitochondrial RCR in group III significantly increased when compared with group II (P < 0.05). These results revealed that the aflatoxin B(1) significantly induced hepatic mitochondrial dysfunction in the activities of hepatic mitochondrial respiratory chain complexes I-IV and the RCR in ducklings. However, sodium selenite could significantly ameliorate the negative effect induced by aflatoxin B(1).

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“…The reason for this is the high metal (zinc, iron, and manganese) content of brain tissue, which catalyzes ROS production, the high oxygen production, the relatively low antioxidant content, and the high concentrations of unsaturated fatty acids [8]. Dopamine and glutamate metabolism is another source of high ROS production [9].…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress and DNA Damage in Untreated First-Episode Psychosis in Adolescents

Şimşek

Gençoğlan

Yüksel³

et al. 2016

Neuropsychobiology

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Objective: Oxidative stress has been reported to play a role in the psychopathology of schizophrenia, though only a few studies have investigated the relationship between early-onset schizophrenia and oxidative stress. The aim of the present study is to evaluate the level of oxidative stress and the presence of DNA damage in first-episode psychosis (FEP) in adolescents. Methods: This study was conducted in the Department of Child Psychiatry of the Dicle University Hospital. It included 20 adolescent patients (age 11-17 years) with psychosis (acute psychosis, schizophreniform disorder, or schizophrenia) according to DSM-IV criteria who had received no previous psychiatric therapy (patient group) and 20 age/gender-matched healthy adolescents (control group). Structured psychiatric interviews [Kiddie Schedule for Affective Disorders and Schizophrenia, Present and Lifetime Version (K-SADS-PL) and Positive and Negative Symptom Scale (PANSS)] were conducted on the patients, and the Clinical Global Impressions (CGI) scale was used to evaluate the severity of disease. Glutathione peroxidase (GPx), superoxide dismutase (SOD), coenzyme Q (CoQ), and 8-hydroxy-2-deoxyguanosine (8-OHdG) levels were determined using the ELISA method and commercial ELISA kits. Results: The mean age was 14.5 ± 1.6 years in the FEP group (male-to-female ratio: 8/12) and 14.4 ± 1.5 years in the control group (male-to-female ratio: 8/12). There were no differences between the patient and control groups in terms of SOD, GPx, or 8-OHdG values (p > 0.05). Conclusions: This study on DNA damage and oxidative stress in FEP in adolescents had a small sample size, and our data suggest that oxidative stress is associated with a chronic disease course rather than being an early sign of early-onset schizophrenia.

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Redox imbalance

Cited by 190 publications

References 142 publications

Influence of Selenium on Hepatic Mitochondrial Antioxidant Capacity in Ducklings Intoxicated with Aflatoxin B1

Influence of Selenium on Hepatic Mitochondrial Antioxidant Capacity in Ducklings Intoxicated with Aflatoxin B1

Protection of Selenium on Hepatic Mitochondrial Respiratory Control Ratio and Respiratory Chain Complex Activities in Ducklings Intoxicated with Aflatoxin B1

Oxidative Stress and DNA Damage in Untreated First-Episode Psychosis in Adolescents

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