• Journal of the Korean Society of Tobacco Science
• /
• v.35 no.1
• /
• pp.56-61
• /
• 2013

Bryonia alba L. belongs to the Cucurbitaceae family and grows in Europe, Asia, America, Africa, Russia, Ukraina and Armenia. The root of Bryonia alba has been used for neuropsychical diseases, psychosis, hysteria, paralysis, epilepsy, vertigo, headache, migrain, melancholia, forgetfulness, sadness, absent mindedness, delirium, cardiovascular disease, ischemia, gastrointestinal diseases, gastric ulcer and respiratory diseases. The root of Bryonia alba contains an oxidized tetra cyclic triterpens, cucurbitaceous, polyunsaturated hydrocarbons, phospholipids, phosphatidylcholines, ethereal oils, fatty acids, a great amount of amino acids, alcohol soluble enzymes, sugar, carotene, vitamin C and E. Bryonia alba increases coronary blood-flow and the amplitude of cardiac contractions. Bryonia alba has an antistressor action and increases the working capacity. Bryonia alba activates connective tissue cells. Bryonia alba markedly increases the oxygen consumption by young and senescent rat brain, liver as well as heart mitochondrial fraction as Korean Ginseng. Bryonia alba decreases lipid peroxidation after immobilization stress. In conclusion, Bryonia alba like Ginseng used in traditional medicine came from ancient time has a good perspective administration as prophylactic and medical remedy, as remedy of lot of diseases in modern medicine.

• Biomolecules & Therapeutics
• /
• v.21 no.3
• /
• pp.210-215
• /
• 2013

Ionizing radiation can induce cellular oxidative stress through the generation of reactive oxygen species, resulting in cell damage and cell death. The aim of this study was to determine whether the antioxidant effects of the flavonoid fisetin (3,7,3',4'-tetrahydroxyflavone) included the radioprotection of cells exposed to ${\gamma}$-irradiation. Fisetin reduced the levels of intracellular reactive oxygen species generated by ${\gamma}$-irradiation and thereby protected cells against ${\gamma}$-irradiation-induced membrane lipid peroxidation, DNA damage, and protein carbonylation. In addition, fisetin maintained the viability of irradiated cells by partially inhibiting ${\gamma}$-irradiation-induced apoptosis and restoring mitochondrial membrane potential. These effects suggest that the cellular protective effects of fisetin against ${\gamma}$-irradiation are mainly due to its inhibition of reactive oxygen species generation.

• Food Science and Biotechnology
• /
• v.15 no.4
• /
• pp.612-616
• /
• 2006

The protective effect of water extract of ash tree leaves (ALE) against oxidative damages was investigated in paracetamol-induced BALB/c mice. Biochemical analysis of anti-oxidative enzymes, immunoblot analyses of hepatic cytochrome P450 2El (CYP2E1), and the gene expression of tumor necrosis factor (TNF-${\alpha}$) were examined to determine the extract's protective effect and its possible mechanisms. BALB/c mice were divided into three groups: normal, paracetamol-administered, and ALE-pretreated groups. A single dose of paracetamol led to a marked increase in lipid peroxidation as measured by malondialdehyde (MDA). This was associated with a significant reduction in the hepatic antioxidant system, e.g., glutathione (GSH). Paracetamol administration also significantly elevated the expression of CYP2E1, according to immunoblot analysis, and of TNF-${\alpha}$ mRNA in liver. However, ALE pretreatment prior to the administration of paracetamol significantly decreased hepatic MDA levels. ALE restored hepatic glutathione and catalase levels and suppressed the expression of CYP2E1 and TNF-${\alpha}$ observed in inflammatory tissues. Moreover, ALE restored mitochondrial ATP content depleted by the drug administration. These results show that the extract of ash tree leaves protects against paracetamol-induced oxidative damages by blocking oxidative stress and CYP2E1-mediated paracetamol bioactivation.

• The Korean Journal of Pharmacology
• /
• v.32 no.2
• /
• pp.201-209
• /
• 1996

Restoration of the blood flow after a period of ischemia is accompanied by generation of toxic oxygen radicals. This phenomenon may account for the occurrence of reperfusion-mediated tissue injury in ischemic hearts. In in vitro studies, although oxygen radicals can be generated from a variety of sources, including xanthine oxidase system, activated leucocytes, mitochondria and others, the most important source and mechanism of oxygen radical production in the post-ischemic reperfused hearts is unclear. In the present study, we tested the hypothesis that the respiratory chain of mitochondria might be an important source of oxygen radicals which are responsible for the development of the reperfusion injury of ischemic hearts. Langendorff-perfused, isolated rat hearts were subjected to 30 min of global ischemia at $37^{\circ}C$, followed by reperfusion. Amytal, a reversible inhibitor of mitochondrial respiration, was employed to assess the mitochondrial contributions to the development of the reperfusion injury. Intact mitochonria were isolated from the control and the post-ischemic reperfused hearts. Mitochondrial oxygen radical generation was measured by chemiluminescence method and the oxidative tissue damage was estimated by measuring a lipid peroxidation product, malondialdehyde(MDA). To evaluate the extent of the reperfusion injury, post-ischemic functional recovery and lactate dehydrogenase(LDH) release were assessed and compared in Amytal-treated and -untreated hearts. Upon reperfusion of the ischemic hearts, MDA release into the coronary effluent was markedly increased. MDA content of mitochondria isolated from the post-ischemic reperfused hearts was increased to 152% of preischemic value, whereas minimal change was observed in extramitochondrial fraction. The generation of superoxide anion was increased about twice in mitochondria from the reperfused hearts than in those from the control hearts. Amytal inhibited the mitochondrial superoxide generation significantly and also suppressed MDA production in the reperfused hearts. Additionally, Amytal prevented the contractile dysfunction and the increased release of LDH observed in the reperfused hearts. In conclusion, these results indicate that the respiratory chain of mitochondria may be an important source of oxygen radical formation in post-ischemic reperfused hearts, and that oxygen radicals originating from the mitochondria may contribute to the development of myocardial reperfusion injury.

• Reproductive and Developmental Biology
• /
• v.33 no.4
• /
• pp.273-281
• /
• 2009

Antioxidants partially ameliorated the detrimental effects of reactive oxygen species (ROS) on sperm characteristics during in vitro storage. The objective of the present study was to investigate the single or synergetic antioxidative effect of curcumin and Vit. E on the characteristics of fresh boar sperm during in vitro storage. The sperm viability in curcumin, Vit. E supplementation and curcumin+Vit. $E+H_2O_2$ groups remained over 85.0% in 3 hr incubation period, but in 6 hr incubation period, curcumin+Vit. $E+H_2O_2$ groups was sharply dropped than those of curcumin and Vit. E group. The membrane intergrity in all evaluated groups except for $H_2O_2$ group did not significantly difference in 3 hr incubation period. The viability in curcumin or Vit. E supplementation were significantly increased than in curcumin+$H_2O_2$ and Vit. $E+H_2O_2$ group in 6 hr incubation period. The percentage of mitochondrial activity and acrosome intergrity obtained similar trends within same incubation periods irrespective of treatment. The lipid peroxidation of spermatozoal plasma membrane ranged from $11.6{\sim}17.5\;nM/l{\times}10^6$ and $14.0{\sim}19.0\;nM/l{\times}10^6$ in 3 hr and 6 hr incubation periods. In conclusion, curcumin or Vit. E surpplementation alone or cooperatively improved sperm viability index (motility, membrane intergrity, viability and survival rates) and fertility index (mitochondria activity, acrosome intergrity and lipid peroxidation) of fresh boar sperm, indicating that curcumin and Vit. E have a antioxidative properties through its scavenging activity against hydrogen peroxide.

• Journal of Life Science
• /
• v.23 no.7
• /
• pp.904-912
• /
• 2013

This study aimed to evaluate the protective effect of cordycepin-increased Cordyceps militaris strain on carbon tetrachloride ($CCl_4$)-induced hepatotoxicity and oxidative stress in rats. Male Sprague-Dawley rats were randomly divided into five groups (n=6) based on six dietary categories: normal (N), $CCl_4$ control (C), $CCl_4$ plus Paecilomyces japonica (CPJ) (3%, w/w), $CCl_4$ plus C. militaris (CCM) (3%, w/w), and $CCl_4$ plus cordycepin-increased C. militaris ($CCM{\alpha}$) (3%, w/w). The activities of the liver marker enzymes ALT, AST, and LDH and the levels of lipid peroxidation were increased in the $CCl_4$-treated groups, but these parameters were significantly decreased in the $CCM{\alpha}$ group. The TBARS content in the liver homogenate, microsome, and mitochondrial fractions of the C group was significantly elevated compared with the N group. However, in the $CCl_4$-treated groups, $CCM{\alpha}$ group was significantly lowered in the TBARS levels of hepatic homogenate and microsomal fractions. The C group showed a significant decrease in the levels of plasma and hepatic glutathione, whereas they were significantly increased in the $CCM{\alpha}$ group. Accordingly, cordycepin-increased C. militaris may be an ideal animal model for studying hepatoprotective effects.

• Journal of Nutrition and Health
• /
• v.24 no.4
• /
• pp.299-307
• /
• 1991

The present study was designed to evaluate the effects of dietary coenzyme $Q_{10}$ on mitochondrial coenzyme $Q_{10}$ and fatty acid composition in adriamycin (ADR)-treated rats. Two experiments were conducted in rats. Experiment 1 was undertaken under the condition of simultaneous administration of ADR and coenzyme $Q_{10}$ for 4 weeks. Experiment 2 was undertaken under the same condition as experiment 1 after feeding the experimental diets alone without administration of ADR for 4 weeks. Heart mitochondrial coenzyme $Q_{10}$ level of rats was greatly decreased by ADR treatment. but higher level of dietary coenzyme $Q_{10}$ elevated this decrease to control ranges. Pretreatment with dietary supplementation of coenzyme $Q_{10}$ showed a significant increase in myocardial coenzyme $Q_{10}$ level. With ADR treatment. polyunsaturated fatty acids such as arachidonic acid (20 : 4) and docosahexaenoic acid (22 : 6) were decreased. However, dietary supplementation of coenzyme $Q_{10}$ modified this decrement to some extent. In both experiment 1 and 2. the polyunsaturated fatty acids/saturated and polyunsaturated fatty acids (P/S+ M) ratio of ADR-treated rats tended to be lower than that of control rats.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.26 no.4
• /
• pp.682-688
• /
• 1997

This study was performed to investigate whether ascorbic acid can modulate the induction of CYP2E1 and prevent the lipid peroxidation which may cause diabetic chronic complication. Diabetes was induced by intraperitoneal injection of streptozotocin to 5-week-old male Sprague-Dawley rats(150~170g). Normal and diabetic group was randomly divided into three groups each; Control(CON, no supplementation), SUP1 (50mg/d ascorbate supplementation) and SUP2(250mg/d ascorbate supplementation). Ascobic acid was prepared daily by dissolving in drinking water and supplied for 4 weeks. There was no difference in hepatic microsomal and mitochondrial P450 contents between normal and diabetes. Hepatic microsomal N-nitrosodimethylamine(NDMA) demethylase activity, which repre-sents contents of CYP2E1, was elevated in diabetes, but not significantly. The NDMA demethylase activity of diabetic SUP2 group was significantly lower activity than that of the diabetic CON group. However, no difference in hepatic mitochondrial NDMA demethylase activity was observed between the diabetes and the normal group. The result suggests that the induction of CYP2E1 in diabetes can be alleviated by ascorbic acid supplementation at the dose of 50mg1d. In addition, ascorbic acid supplementation showed dose-dependent reduction of hepatic microsomal TBARS contents in diabetic rats.

• Animal Bioscience
• /
• v.35 no.10
• /
• pp.1616-1627
• /
• 2022

Objective: This work was conducted to investigate the effects of oxidative stress on meat quality, mitochondrial function, calcium metabolism and ferroptosis of broilers. Methods: In this study, a total of 144 one-day-old male Ross 308 chicks were divided into 3 groups (control group, saline group, and hydrogen peroxide [H₂O₂] group) with 6 replicates of 8 broilers each. The study lasted for 42 d. The broilers in the saline and H₂O₂ groups were intraperitoneally injected with 0.75% saline and 10.0% H₂O₂ on the 16th and 37th day of the experimental period respectively, the injection volumes were 1.0 mL/kg of broiler body weight. On the 42nd day of the experimental period, two chicks were randomly selected from each cage, a total of thirty-six chicks were stunned by electric shock and slaughtered to collect breast muscle samples. Results: The H₂O₂ exposure reduced pH value, increased drip loss and shear force of breast meat (p<0.05), impaired the ultrastructure and function of mitochondria. The H₂O₂ exposure damaged the antioxidant system in mitochondria, excessive reactive oxygen species carbonylation modified calcium channels on mitochondria, which impaired the activities of key enzymes on calcium channel, resulted in the increased calcium concentration in cytoplasm and mitochondria (p<0.05). In addition, the H₂O₂ exposure increased the iron content and lipid peroxidation (p<0.05), which induced ferroptosis. Conclusion: Oxidative stress could impair meat quality by causing mitochondrial dysfunction, resulting in calcium metabolism disorder and ferroptosis.

• Animal Bioscience
• /
• v.37 no.6
• /
• pp.1001-1006
• /
• 2024

Objective: This study aimed to investigate the effect of Codonopsis pilosula polysaccharide (CPP) on the motility, mitochondrial integrity, acrosome integrity rate, and antioxidant ability of sheep sperm after preservation at 4℃. Methods: Semen from healthy adult rams were collected and divided into four groups with separate addition of 0, 200, 400, and 1,000 mg/L CPP. Sperm motility was analyzed using the Computer-Assisted Semen Analysis software after preservation at 4℃ for 24, 72, 120, and 168 h. Sperm acrosome integrity rate was analyzed by Giemsa staining at 24, 72, and 120 h, and mitochondrial membrane integrity was analyzed by Mito-Tracker Red CMXRos. The total antioxidant capacity (T-AOC) and malondialdehyde (MDA) content of spermatozoa were measured after 120 h of preservation. Results: The sperm viability and forward-moving sperm under 200 mg/L CPP were significantly higher than that in the control group at 72 h (61.28%±3.89% vs 52.83%±0.70%, 51.53%±4.06% vs 42.84%±1.14%), and 168 h (47.21%±0.85% vs 41.43%±0.37%, 38.68%±0.87% vs 31.68%±0.89%). The percentage of fast-moving sperm (15.03%±1.10% vs 11.39%±1.03%) and slow-moving sperm (23.63%±0.76% vs 20.29%±1.11%) in the 200 mg/L group was significantly higher than control group at 168 h. The mitochondrial membrane integrity of the sperm in the group with 200 mg/L CPP was significantly higher than those in the control group after storage at 4℃ for 120 h (74.76%±2.54% vs 65.67%±4.51%, p<0.05). The acrosome integrity rate in the group with 200 mg/L (87.66%±1.26%) and 400 mg/L (84.00%±2.95%) was significantly higher than those in the control group (80.65%±0.16%) after storage for 24 h (p<0.05). CPP also increased T-AOC and decreased the MDA concentration after preservation at 4℃ (p<0.05). Conclusion: Adding CPP could improve the T-AOC of sperm, inhibit lipid peroxidation, and facilitate semen preservation.