• Korean Journal of Food Science and Technology
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• v.30 no.5
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• pp.1222-1228
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• 1998

Stress will induce various changes in human metabolism. The remarkable phenomenon of these changes is increased energy metabolism that can induce many reactive oxygen species (ROS) production. ROS can peroxidize cellular macromolecules including lipid and protein. The object of this study was to investigate that stress may induce cellular damage by producing ROS and that Rooibos tea can protect cells against reactive oxygen species by immobilization stress in SD rat. The stress group significantly increased in 5-hydroxyindole acetic acid (5-HIAA), one of the stress hormone. Rooibos tea treatment had no effects on 5-HIAA contents, but body weight of Rooibos tea treated rat more increased than that of only the stress group. It was suggested that Rooibos tea colud not affect stress response itself, but protect against the another mechanism. We thought that the oxidative damage was caused by increased energy metabolism. Protein degradation level and lipid peroxide formation on index of oxidative damage significantly increased in the stress group. But the stress-induced activity change could not be observed in antioxidative enzymes such as superoxide dismutase, glutathione peroxidase and glutathione reductase. But the catalase activity of the brain significantly was inhibited by the stress. From these results, it was suggested that the immobilization stress induce the brain oxidative damage. However the oxidative damage was inhibited by feeding Rooibos tea containing various antioxidants, such as polyphenol, flavonoid and so on. Therefore, Rooibos tea have the protective effects against the stress caused by the ROS mediated cellular damage.

• Environmental Analysis Health and Toxicology
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• v.15 no.3
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• pp.61-67
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• 2000

Toxic lesions of styrene in the Japanese Medaka (Oryzias latipes) were compared with those of styrene oxide, the active metabolite of styrene, using embryo-larval assays. The developmental stages of Japanese Medaka (Oryzias latipes) treated with both chemicals were not altered and progressed normally. However, styrene oxide was more toxic than styrene in terms of causing death and lesions . High concentrations of styrene (higher than 4.9 ppm) and styrene oxide (higher than 2.4 ppm), resulting in more than 50% mortality, caused similar lesions of cardiovascular system, craniofacial bone formation and spinal deformities, although a number of lesions were not observed by both chemicals . In the group treated with styrene, eyeball sizes and intereye distances were reduced, while, in the group treated with styrene oxide , the eyes and eye cups were not developed and two eyes were sometimes fused. In addition, styrene oxide caused the lesion which involved the posterior brain and brain stem were herniated through the spinal cord . The noticeable difference of toxic symptoms between these two chemicals was the time of onset. Toxicities of cardiovascular system and craniofacial bone formation appeared on day 3 of development in styrene oxide treated group, but, styrene treated group staned to show hemorrhages on day 3 and the craniofacial malformation were appeared on day 5, These differences between two chemicals may be due to the metabolism of styrene to styrene oxide, the reactive intermediate.

• Journal of the Korean Institute of Oriental Medical Informatics
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• v.19 no.2
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• pp.1-20
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• 2013

This research observed the interrelations between the active components found specifically in red ginseng and fermented red ginseng from among the variety of ginseng variations and the protective effect and anti-oxidant effect exercised on brain cells in the animal model for MPTP-induced neurotoxic Parkinson's Disease and obtained the following conclusions. The results above comprehensively demonstrated that the fermented red ginseng extract exercised greater protective effects against oxidant brain damage by MPTP when compared to the group administered with the red ginseng extract. This was induced an increase in TH protein expression, and further raised the efficiency of the anti-oxidant enzyme defensive system against neurotoxicity, thereby restraining the lipid peroxidation caused by the active oxygen generated during the course of MPTP metabolism and enhancing the body's defensive capacities in response to tissue damage, thereby demonstrating a protective effect against MPTP induced neurotoxicity.

• Biomedical Science Letters
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• v.12 no.4
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• pp.355-359
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• 2006

This investigation was performed to study the antioxidant activities of Cornus officinalis Sieb extracts and the effect of Cornus officinalis Sieb extracts on glucose, lipid metabolism in diabetic rats. DPPH free radical scavanging activity and superoxide anion radical scavenging of Cornus officinalis Sieb extracts were 94.7% and 92.1%, respectively. Streptozotocin (45 mg/kg body weight, i.p.) induced diabetic rats showed a significant increases of plasma glucose, triglyceride and total cholesterol, concomitantly significant decrease of plasma high density lipoprotein. Glutathione level were decrease in cytosol of liver, lung and brain tissue of rats. Lipid peroxide were increase in microsome of liver cells. Group 1 and 2 were treated with Cornus officinalis Sieb extracts 200 mg/kg body weight and 100 mg/kg body weight for 24 days, individually. Group 1 and 2 rats showed decreased plasma glucose, triglyceride, total cholesterol and lipid peroxide in microsome of liver, and increased plasma high density lipoprotein and glutathione in cytosol of liver, lung and brain. The result suggest that Cornus officinalis Sieb extracts may normalize the Impaired antioxiants status in streptozotocin induced diabetic rats. Cornus officinalis Sieb extracts were used to improve the imbalance between free radicals and antioxidant system due to the diabetes.

• Journal of Society of Preventive Korean Medicine
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• v.4 no.1
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• pp.122-131
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• 2000

This dissertation is try to figure out why chestnut belongs to kidney channel, from the viewpoint of five elements theory. After studying chestnut's property, flavor, channel tropism, main cure ability, prescriptions, shape, sweet, and prohibitions, I came to the following results. 1. Property of chestnut is warm and has no toxicity, so it is less related than kidney property. 2. Flavor of chestnut is salty and sweet, so it has some relation to kidney and spleen properties. 3. Channel tropism of chestnut enters mainly into kidney channel, and then spleen and stomach channels. 4. Chestnut controls kidney function of storing the essence of life, determining the condition of bone and marrow, conduction water metabolism, affecting reasoning activity, and controls activity of nine openings of body. It also has effects on functions of spleen, intestines and stomach. 5. Prescriptions including chestnut is similar to that of human brain, it is possible to reason out that chestnut has some relation to human brain. 7. As flavor of chestnut flower is similar to that of spermatic fluid, so it has som relation to kidney property. 8. As chestnut has property of blocking qi and it causes spleen, stomach and colon system to be confused, so it is suggested that persons with weakende spleen and stomach be not allowed to take in.

• Journal of Pharmacopuncture
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• v.23 no.1
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• pp.1-7
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• 2020

Nicotine, primary component of tobaco produces craving and withdrawal effect both in humans and animals. Nicotine shows a close resemblance to other addictive drugs in molecular, neuroanatomical and pharmacological, particularly the drugs which enhances the cognitive functions. Nicotine mainly shows its action through specific nicotinic acetylcholine receptors located in brain. It stimulates presynaptic acetylcholine receptors thereby enhancing Ach release and metabolism. Dopaminergic system is also stimulated by it, thus increasing the concentration of dopamine in nuclear accumbens. This property of nicotine according to various researchers is responsible for reinforcing behavioral change and dependence of nicotine. Various researchers have also depicted that some non dopaminergic systems are also involved for rewarding effect of nicotinic withdrawal. Neurological systems such as GABAergic, serotonergic, noradrenergic, and brain stem cholinergic may also be involved to mediate the actions of nicotine. Further, the neurobiological pathway to nicotine dependence might perhaps be appropriate to the attachment of nicotine to nicotinic acetylcholine receptors, peruse by stimulation of dopaminergic system and activation of general pharmacological changes that might be responsible for nicotine addiction. It is also suggested that MAO A and B both are restrained by nicotine. This enzyme helps in degradation dopamine, which is mainly responsible for nicotinic actions and dependence. Various questions remain uninsurable to nicotine mechanism and require more research. Also, various genetic methods united with modern instrumental analysis might result for more authentic information for nicotine addiction.

• YAKHAK HOEJI
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• v.32 no.5
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• pp.343-350
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• 1988

Recent hypothesis suggested that intracellular accumulation of calcium is a common denominator of ischemic celullar damage. Flunarizine, a calcium entry blocker, posses vasodilating properties in cerebral vascular beds and clinically used in circulatory disorders. The present study was designed to evaluate the effect of flunarizine on ischemic and hypoxic brain damage. An ischemic model was made by bilateral carotid artery ligation (BCAL) in Wistar strain rat. Hypoxic model was made by intravenous injection(i.v.) of KCN to rats and mice. In mice, flunarizine not only reduced the mortality of KCN, but also delayed the onset time of convulsion. The contents of ATP, creatine phosphate and glucose, cerebral energy metabolite, decreased 30 minutes after BCAL and KCN i, v, while that of lactate increased. But these variations were suppressed by flunarizine. Furthermore, increase in the dosage of flunarizne generally promoted the recovery of cerebral energy metabolites in hypoxic animals. The results suggest that flunarizine had a protective effect against ischemic and hypoxic brain damage due to its ameliorating action on the cerebral energy metabolism.

• Korean Journal of Pharmacognosy
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• v.23 no.2
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• pp.106-114
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• 1992

The acute toxicity and the effect of steam distillate obtained from several plant mixtures (G-3) on the reactivation of brain, lung, and blood acetylcholinesterase (AChE) activity, and recovery from other toxic symptoms following intoxication by organophosphate pesticides were investigated in mice and mudfish. Administration of G-3 $(50{\sim}100\;ml/kg,\;i.p.)$ immediately or 30 min prior to Diazinon or Sumithion treatments, respectively, resulted in a significant reactivation of AChE activity in brain, lung, and blood, their potencies being almost equipotent to those of 2-PAM, one of well-known antidotes. G-3 itself exhibited almost no acute toxicity even at the highest dose employed, and without effect on the inhibition of hepatic drug metabolism function following organophosphate administrations. G-3 showed a significant diminution of the death rate in mudfish as well as in mice intoxicated by Diazinon.

• Proceedings of the Korea Society of Environmental Toocicology Conference
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• 1996.12a
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• pp.25-41
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• 1996

KWON, O. S. SCHMUED, L. C. and LSIKKER, W. JR. Neurotoxiciligy. objectives of this study were to test the hypothesis that fumonisin $B_1$ ($FB_1$) alters sphinganine (Sa) levels and myelin synthesis in the central nervous system of developing rats. $FB_1$ (subcutaneous, 0. 4 or 0. 8 mg/kg/day) from postnatal days (PND) 3 to PND 12 resulted in a significantly increased in the brain of rats given 0. 8 mg $FB_1$/kg/day. To confirm the effect of limited nutrition on changes in the Sa levels and myelinogenesis, rats given 0.8mg $FB_1$/kg/day or treated by limited nutrition (temporary removal from dam during postnatal period) were compared to those in saline controls. Sa levels and Sa/So ratios were compared to those in saline in the 0.8 $FB_1$-treated, 3'-phosphohydrolase (CNP) activities were decreased significantly in both nutritionally limited and $FB_1$-exposed rats. These data indicate that sphingolipid metabolism in the central nervous system of develiping rats is vulnerable to $FB_1$ exposure. The hypomyelination associated with $FB_1$-treatment may be mediated by limited nutrition.

• Radiation Oncology Journal
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• v.22 no.4
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• pp.298-306
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• 2004

Purpose: The purpose of this study was to identify Radiosensitivity of proteins in tissues with different radiosensitivity. Materials and Methods: C3H/HeJ mice were exposed to 10 Gy. The mice were sacrifiud 8 hrs after radiation. Their spleen and liver tissues were collected and analyzed histologicaly for apoptosis. The expressions of radiosusceptibillty protein were analyzed by 2-dimensional electrophoresis and matrix-assisted laser desorption ionization time-of-flight mass spectrometry. Resilts: The Peak of apoptosis levels were $35.3{\pm}1.7{\%}$ in spleen and $0.6{\pm}0.2{\%}$ in liver at 8 hrs after radiation. Liver, radioresistant tissues, showed that the levels of ROS metabolism related to proteins such as cytochromm c, glutathione S transferase, NADH dehydrogenase, riken cDNA and peroxiredoxin Vl increased after radiation. The expression of cytochrome c increased significantly in spleen and liver tissues after radiation. In spleen, radiosensitivity tissue, the identified proteins showed a significantly quantitative alteration following radiation. It was categorized as signal transduction, apoptosis, cytokine, Ca signal related protein, stress-related protein, cytoskeletal regulation, ROS metabolism, and others. Conclusion: Differences of radiation-induced apoptosis by tissues specifted were coupled with the induction of related radiosensitivity and radioresistant proteins. The result suggests that apoptosis relate protein and redox proteins play important roles in this radiosusceptibility.