rutin and Body-Weight

rutin has been researched along with Body-Weight* in 13 studies

Trials

1 trial(s) available for rutin and Body-Weight

ArticleYear
Time course of the anti-oedematous effect of O-(beta-hydroxyethyl)-rutosides in healthy volunteers.
    European journal of clinical pharmacology, 1991, Volume: 40, Issue:6

    O-(beta-hydroxyethyl)-rutosides (HR) is used for the treatment of disorders of the venous and microcirculatory systems. In order to evaluate the time course of its activity, the effect of HR on a provocation model of orthostatic oedema in healthy volunteers was used. After a 2 week placebo run-in period, 16 healthy volunteers were randomized to HR (2 tablets of 500 mg/day) of placebo for a further 3 weeks, in a double-blind parallel design. Oedema was provoked by standing motionless for 1 h, with measurement of leg volume before and afterwards. The procedure was undertaken at entry to the study and then weekly during the entire 5 week period. There were no significant differences in the extent of oedema produced by the orthostatic challenge during the 2 week run-in period or in the subjects who continued on placebo (approximately 90 arbitrary units i.e. approximately 48 ml). During the 3 week treatment with HR, however, there was a progressive reduction (-1.1, -5.9, and -7.6 arbitrary units after 1, 2, and 3 weeks, respectively) in the volume of induced oedema, which was significant after 2 and 3 weeks of treatment compared to the placebo group.

    Topics: Adult; Body Weight; Double-Blind Method; Edema; Humans; Hydroxyethylrutoside; Leg; Male; Posture

1991

Other Studies

12 other study(ies) available for rutin and Body-Weight

ArticleYear
Troxerutin protects against DHT-induced polycystic ovary syndrome in rats.
    Journal of ovarian research, 2020, Sep-13, Volume: 13, Issue:1

    The exact pathogenesis of polycystic ovary syndrome (PCOS), the most common neuroendocrine disorder in women of reproductive age, has not been fully elucidated. Recent studies suggested that chronic inflammation and neurotransmitter disorder involved in the progress of PCOS. Troxerutin, a natural flavonoid, was reported to possess neuroprotective effect in several disease models by inhibiting inflammation or enhancing neurotrophic factor. In this study, we investigated the possible protective effect and mechanism of troxerutin in a dihydrotestosterone (DHT)-induced rat model of PCOS. The PCOS rat models were treated with troxerutin at a dose of 150 mg/kg or 300 mg/kg for up to 4 weeks. Results showed that 300 mg/kg troxerutin significantly decreased the body weight gain and improved the pathological changes of ovary induced by DHT. Meanwhile, the elevated gonadotrophin-releasing hormone (GnRH), gonadotrophin and testosterone in the serum of PCOS rats were reduced with the treatment of troxerutin. The expression of kisspeptin and NKB in arcuate nucleus and their receptors kiss1r and NK3r in GnRH positive neurons of median eminence were markedly decreased in troxerutin-treated rats. Of note, the GnRH inhibitory regulator GABA and stimulatory regulator glutamate were also restored to the normal level by troxerutin. The present study indicated that troxerutin may exhibit a protective effect in PCOS rat model via regulating neurotransmitter release.

    Topics: Animals; Body Weight; Dihydrotestosterone; Disease Models, Animal; Dose-Response Relationship, Drug; Drug Administration Schedule; Female; Gene Expression Regulation; Gene Regulatory Networks; Gonadotropin-Releasing Hormone; Gonadotropins; Hydroxyethylrutoside; Polycystic Ovary Syndrome; Rats; Testosterone

2020
Anti-arrhythmogenic and anti-inflammatory effects of troxerutin in ischemia/reperfusion injury of diabetic myocardium.
    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2018, Volume: 102

    Medicinal plants are increasingly used in the treatment of cardiovascular diseases due to their multifaceted properties. This study was designed to investigate anti-arrhythmic and anti-inflammatory potentials of the natural bioflavonoid, troxerutin (TXR) in myocardial ischemia/reperfusion (I/R) injury in diabetic rats.. Male Wistar rats were randomly divided into 4 groups (control, control + TXR [150 mg/kg, daily], diabetic, and diabetic + TXR). Type-1 diabetes was induced by an intraperitoneal injection of streptozotocin (50 mg/kg) and lasted for 10 weeks. After mounting on the Langendorff apparatus, isolated hearts in all groups received a normal Krebs-Henseleit solution for 20 min of stabilization period, followed by 30 min of regional ischemia through ligation of the left anterior descending coronary artery, and 60 min of full reperfusion. During the experiment, the electrocardiograms were recorded and the arrhythmias [number, duration and incidence of premature ventricular complexes (PVC), ventricular tachycardia (VT), ventricular fibrillation (VF), and arrhythmia score] during I/R phases were assessed based on the Lambeth Convention. Ischemic left ventricular samples were used to determine the activities of lactate dehydrogenase (LDH), interleukin-1beta (IL-1β), and tumor necrosis factor (TNF-α).. The arrhythmias induced by I/R were not significantly changed in diabetic group as compared to the control group. However, pretreatment with TXR significantly reduced the number of PVC and duration and incidence of VF in ischemic phase in comparison to the untreated animals (P < 0.05). In addition, the duration, and incidence of most arrhythmias during reperfusion phase were significantly declined by TXR administration in both control and diabetic groups (P < 0.05). Pretreatment of rats with TXR significantly reduced myocardial inflammatory cytokines TNF-α and IL-1β levels after I/R insult in diabetic as well as control hearts (P < 0.05).. Preconditioning with TXR could provide cardioprotection by anti-arrhythmic and anti-inflammatory effects against I/R injury in rat hearts. This effect of TXR can introduce this material as a protective agent in cardiovascular diseases.

    Topics: Animals; Anti-Arrhythmia Agents; Anti-Inflammatory Agents; Blood Glucose; Body Weight; Cytokines; Diabetes Mellitus, Experimental; Electrocardiography; Hydroxyethylrutoside; L-Lactate Dehydrogenase; Male; Myocardial Reperfusion Injury; Myocardium; Rats, Wistar

2018
Troxerutin protects against diabetic cardiomyopathy through NF‑κB/AKT/IRS1 in a rat model of type 2 diabetes.
    Molecular medicine reports, 2017, Volume: 15, Issue:6

    Troxerutin is a bioflavonoid, which can be used to treat venous disorders, thrombosis and cerebrovascular diseases. Recent studies have demonstrated that it may also be used to prevent edemas. However, it is not known whether troxerutin protects against the cardiomyopathic complications of diabetes. In the present study, a rat model of type 2 diabetes was used to investigate the potential for troxerutin to protect against diabetic cardiomyopathy, through changes to nuclear factor‑κB (NF‑κB) expression. Troxerutin administration significantly reduced heart rate, blood pressure, blood glucose and plasma triglyceride levels across all measured time points. Furthermore, troxerutin significantly reduced reactive oxygen species levels, NF‑κB protein expression, and suppressed the phosphorylated forms of AKT, insulin receptor substrate 1 (IRS1) and c‑Jun N‑terminal kinase (JNK). These results suggested that troxerutin protects against cardiomyopathy via alterations in NF‑κB, AKT and IRS1 signaling, in a rat model of type 2 diabetes.

    Topics: Animals; Biomarkers; Blood Glucose; Body Weight; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 2; Diabetic Cardiomyopathies; Disease Models, Animal; Hydroxyethylrutoside; Insulin Receptor Substrate Proteins; JNK Mitogen-Activated Protein Kinases; Male; NF-kappa B; Proto-Oncogene Proteins c-akt; Rats; Reactive Oxygen Species; Signal Transduction

2017
Antidiabetic effect, antioxidant activity, and toxicity of 3',4'-Di-O-acetyl-cis-khellactone in Streptozotocin-induced diabetic rats.
    Bioorganic & medicinal chemistry letters, 2016, 08-15, Volume: 26, Issue:16

    Pyranocoumarins are compounds with an important pharmacological profile, such as anti-inflammatory, antioxidant, cytotoxic, antiviral, antibacterial, and hypoglycemic effects. These molecules have a widespread presence as secondary metabolites in medicinal plants used to treat Diabetes Mellitus (DM). The aim of this work was to evaluate antidiabetic activity in Streptozotocin (STZ)-induced diabetic rats and the antioxidant effects of 3',4'-Di-O-acetyl-cis-khellactone (DOAcK), as well as its toxic potential. We obtained DOAcK with an enantiomeric excess of 70% by chemical synthesis. Our results showed that this compound exerts an important antidiabetic effect: blood glucose decreased in groups treated with DOAcK by 60.9% at dose of 15mg/kg (p<0.05) compared with the diabetic control group, and demonstrated a statistically significant increase in weight gain (45.7±9.7 in the group treated with DOAcK vs. -23.0±33.1 in the group with diabetes). In a biochemical profile, DOAcK did not modify lipid metabolism and did not cause damage at the renal level. DOAcK administration increased the activities of Catalase (CAT), Glutathione Peroxidase (GPx), and Super Oxide Dismutase (SOD) to levels near those of the healthy group. Histopathological analysis exhibited morphology similar to that of the healthy group and the group treated with DOAcK. DOAcK is not mutagenic by Ames test for Salmonella typhimurium strains TA98, TA100, or TA102, and is not genotoxic by Micronucleus assay; median lethal dose (LD50) >2000mg/kg and, at this dose, no signs of toxicity or death were reported after 14days of observation. These results indicate that DOAcK can improve glucose metabolism, which may be due to the increased antioxidant activity of CAT, GPx and SOD. In addition, DOAcK is not toxic in the studies tested.

    Topics: Animals; Antioxidants; Blood Glucose; Body Weight; Catalase; Coumarins; Diabetes Mellitus, Experimental; Glutathione; Glutathione Peroxidase; Hypoglycemic Agents; Insulin; Islets of Langerhans; Liver; Mutagenicity Tests; Oxidative Stress; Rats; Salmonella typhimurium; Streptozocin; Superoxide Dismutase

2016
Troxerutin protects against high cholesterol-induced cognitive deficits in mice.
    Brain : a journal of neurology, 2011, Volume: 134, Issue:Pt 3

    Recent findings suggest that neurotoxicity is the mechanism underlying the induction of neuronal insulin resistance by a high cholesterol diet. Troxerutin, a naturally occurring flavonoid, has been reported to possess biological activity beneficial to human health. Our recent studies have demonstrated that troxerutin attenuates cognitive impairment and oxidative stress induced by D-galactose in mouse brain through decreasing advanced glycation end products, reactive oxygen species and protein carbonyl levels and enhancing phosphoinositide 3-kinase/Akt activation. In this study, we evaluated the effect of troxerutin on cognitive impairment induced by brain insulin resistance in mice fed a high-cholesterol diet, and explored its potential mechanism. Our results showed that oral administration of troxerutin to these mice significantly improved behavioural performance in a step-through passive avoidance task and a Morris water maze task, at least in part, by decreasing the levels of reactive oxygen species, protein carbonyl and advanced glycation end products and blocking endoplasmic reticulum stress via reduced phosphorylation of the pancreatic endoplasmic reticulum-resident kinase and eukaryotic translation initiation factor 2α. Furthermore, troxerutin significantly inhibited the activation of c-jun N-terminal kinase 1 and IκB kinase β/nuclear factor-κB induced by endoplasmic reticulum stress and enhanced insulin signalling pathway, which prevented obesity, restored normal levels of blood glucose, fatty acids and cholesterol and increased the phosphorylation of cyclic adenosine monophosphate response element-binding protein and the expression levels of c-fos in the hippocampus. Moreover, troxerutin significantly inhibited endoplasmic reticulum stress-induced apoptosis and decreased the activation of caspase-12 and caspase-3, and reduced the mean optical density of the terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick end label-positive cells in the hippocampus. However, intra-cerebroventricular infusion of PI-103, a specific phosphoinositide 3-kinase 110α inhibitor, significantly inhibited the expression levels of phosphoinositide 3-kinase 110α and phosphoinositide 3-kinase downstream signalling in the hippocampus of mice co-treated with high cholesterol and troxerutin and vehicle control mice. These results suggest that troxerutin could be recommended as a possible candidate for the prevention and therapy of cognitive deficits in typ

    Topics: Animals; Avoidance Learning; Blood Glucose; Body Weight; Brain; Cholesterol; Cognition Disorders; CREB-Binding Protein; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay; Fatty Acids, Nonesterified; Gene Expression Regulation; Glycation End Products, Advanced; Hydroxyethylrutoside; Immunoprecipitation; In Situ Nick-End Labeling; Infusions, Intraventricular; Insulin Resistance; Male; Maze Learning; Mice; Mice, Inbred C57BL; Neuroprostanes; Phosphorylation; Protein Carbonylation; Reactive Oxygen Species; Signal Transduction; Triglycerides

2011
Troxerutin protects the mouse liver against oxidative stress-mediated injury induced by D-galactose.
    Journal of agricultural and food chemistry, 2009, Sep-09, Volume: 57, Issue:17

    Troxerutin, a trihydroxyethylated derivative of rutin, has been well-demonstrated to exert hepatoprotective properties. In the present study, we attempted to explore whether the antioxidant and anti-inflammatory mechanisms were involved in troxerutin-mediated protection from D-gal-induced liver injury. The effects of troxerutin on liver lipid peroxidation, antioxidant enzymatic activities, and the expression of inflammatory mediator were investigated in D-gal-treated mice. The results showed that troxerutin largely attenuated the D-gal-induced TBARS content increase and also markedly renewed the activities of Cu, Zn-SOD, CAT, and GPx in the livers of D-gal-treated mice. Furthermore, troxerutin inhibited the upregulation of the expression of NF-kappaB p65, iNOS, and COX-2 induced by D-gal. D-Gal-induced tissue architecture changes and serum ALT and AST increases were effectively suppressed by troxerutin. In conclusion, these results suggested that troxerutin could protect the mouse liver from D-gal-induced injury by attenuating lipid peroxidation, renewing the activities of antioxidant enzymes and suppressing inflammatory response. This study provided novel insights into the mechanisms of troxerutin in the protection of the liver.

    Topics: Alanine Transaminase; Animals; Anti-Inflammatory Agents; Antioxidants; Aspartate Aminotransferases; Body Weight; Chemical and Drug Induced Liver Injury; Galactose; Hydroxyethylrutoside; Lipid Peroxidation; Liver; Male; Mice; Oxidative Stress; Transcription Factor RelA

2009
Efficacy of troxerutin on streptozotocin-induced rat model in the early stage of diabetic retinopathy.
    Arzneimittel-Forschung, 2005, Volume: 55, Issue:10

    The vascular changes associated with early diabetic retinopathy, which include the formation of microaneurysms and acellular capillaries, vessel dilation, vascular endothelial growth factor expression, were investigated experimentally in streptozotocin-induced diabetic rats treated with antioxidants: troxerutin (trihydroxy-ethylrutoside, CAS 7085-55-4), Vaccinium myrtillus, and calcium dobesilate (hydroquinone calcium sulfonate, CAS 20123-80-2). The development and progression of retinopathy was followed using fundus photography. After 3 months, the rats were sacrificed and half of the eyes were prepared for neovascularization analysis, and the other half were used for VEGF (vascular endothelial growth factor) analysis. The results from fundus photography and ADPase (adenosine diphosphatase) staining were quantified by the percentage area of the retinal vasculature using a commercial image analyzer. The VEGF protein in the retinal homogenates was assessed using an ELISA (enzyme linked immunosorbent assay) kit and VEGF-mRNA by RT-PCR (reverse transcription polymerase chain reaction). In the ADPase stain, the retinal vascular percent area increased significantly in the diabetic control. Neovascularization and aneurysms were observed in the diabetic control and were attenuated by 50 mg/kg troxerutin, but the retinal vascular percentage area was not significantly different from the diabetic control. The VEGF protein concentration was higher in diabetic rats than in the nondiabetic rats (21.5 +/- 2.1 vs 27.7 +/- 5.8 pg/mg, p < 0.05), and this increase was attenuated by 10 mg/kg troxerutin (24.5 +/- 3.8 pg/mg, p < 0.05) and prevented by 50 mg/kg troxerutin (19.5 +/- 2.2 pg/mg, p < 0.05). However, there were no significant differences between the groups. The VEGF-mRNA density showed a increasing tendency by 20% in the diabetic rats compared with the non-diabetic rats (1.0 +/- 0.1 vs 1.2 +/- 0.1 VEGF/beta-actin), and this increase was corrected by 10 mg/kg troxerutin (1.0 +/- 0.1 VEGF/beta-actin), 50 mg/kg troxerutin (0.9 +/- 0.1 VEGF/beta-actin) and Vaccinium myrtillus (1.1 +/- 0.1 VEGF/beta-actin). Oxidative stress might be involved in the upregulation of retinal VEGF during early diabetes, and it is likely that troxerutin has comparatively effective antioxidant properties. Therefore, troxerutin might be a useful treatment for attenuating diabetic retinopathy.

    Topics: Animals; Apyrase; Blood Glucose; Body Weight; Calcium Dobesilate; Diabetes Mellitus, Experimental; Diabetic Retinopathy; Enzyme-Linked Immunosorbent Assay; Fundus Oculi; Hemostatics; Hydroxyethylrutoside; Phytotherapy; Rats; Reverse Transcriptase Polymerase Chain Reaction; RNA; Vaccinium myrtillus; Vascular Endothelial Growth Factor A; Vasoconstrictor Agents

2005
Cardioprotective properties of O-(beta-hydroxyethyl)-rutosides in doxorubicin-pretreated BALB/c mice.
    Cancer research, 1993, Oct-01, Volume: 53, Issue:19

    Chronic doxorubicin-induced cardiotoxicity is believed to be caused by the formation of oxygen free radicals. Thus O-(beta-hydroxyethyl)-rutosides, a standardized flavonoid mixture (Venoruton) with iron chelating and radical scavenging activity, might provide protection. Therefore, we investigated the (cardio)protective effect of Venoruton (1.5 g/kg injected i.p. on days 1-5, 8-12, 15-19, and 22-26) in BALB/c mice treated with doxorubicin (4 mg/kg injected i.v. on days 1, 8, 15, and 22) compared with mice treated with doxorubicin alone. Saline-treated animals served as controls. No mortality was encountered in either of the groups; weight gain data suggest little general toxicity of this dose schedule. The basal frequency of the isolated right atria was increased in doxorubicin-pretreated animals as compared to control animals (468 +/- 22 and 366 +/- 20 beats/min, respectively). Venoruton coadministration diminished this increase (373 +/- 17 beats/min). The -log of the concentration giving 50% effect of l-isoprenaline on the right atrium was changed after doxorubicin pretreatment (8.33 +/- 0.04 versus 8.86 +/- 0.06 for control animals). Venoruton coadministration resulted in a smaller shift in the -log of the concentration giving 50% effect (8.51 +/- 0.10) than with doxorubicin alone. The extent of cardiotoxicity found in the functional studies was confirmed by histological scoring of heart ventricle damage. It can be concluded that Venoruton has the potential to protect against doxorubicin-induced cardiotoxicity.

    Topics: Animals; Body Weight; Colforsin; Doxorubicin; Drug Administration Schedule; Free Radical Scavengers; Heart; Heart Rate; Hydroxyethylrutoside; Injections, Intraperitoneal; Injections, Intravenous; Isoproterenol; Male; Mice; Mice, Inbred BALB C; Myocardial Contraction; Myocardium; Razoxane; Time Factors

1993
o-(beta-Hydroxyethyl)-rutoside-mediated protection of renal injury associated with cis-diamminedichloroplatinum(II)/hyperthermia treatment.
    Cancer research, 1988, Apr-15, Volume: 48, Issue:8

    A bioflavonoid, o-(beta-hydroxyethyl)-rutoside, has been investigated for its potential to increase the therapeutic index of the combined treatment modalities of whole body hypothermia (WBH) (41.5 degrees C) and chemotherapy (cisplatin) in studies utilizing a transplantable fibrosarcoma solid tumor model in Fischer rats. When whole body WBH was induced 45 min after cisplatin administration, a significantly increased tumor growth delay was noted beyond that achieved by either treatment modality alone. The combination of WBH and cisplatin treatments, however, produced an unacceptable increase in renal injury. o-(beta-Hydroxyethyl)-rutoside administration was found to effectively block the renal injury without interfering with the antitumor efficacy of the combined regimen. Potential explanations for the ability of o-(beta-hydroxyethyl)-rutoside to affect the increase in WBH-cisplatin therapeutic regimen are discussed.

    Topics: Animals; Body Weight; Cisplatin; Free Radicals; Glomerular Filtration Rate; Hydroxyethylrutoside; Hyperthermia, Induced; Kidney; Male; Mice; Mice, Inbred C57BL; Mice, Inbred DBA; Neoplasms, Experimental; Rutin

1988
Protective effects of O-(beta-hydroxyethyl)-rutosides (HR) against adriamycin-induced toxicity in rats.
    Archives internationales de pharmacodynamie et de therapie, 1985, Volume: 273, Issue:2

    Adriamycin (Adriablastine), administered weekly at the dose of 5 mg/kg i.p. for 3 weeks in rats, produced a general decrease of vitality associated with a decrease of body weight, hypothermia, decreases of stroke volume and cardiac output. Hematocrit was decreased. Renal blood flow decreased whereas pulmonary blood flow increased. Mean blood pressure and heart rate remained unaffected. Biochemical evaluations revealed a decrease of blood urea and serum creatinine, which might be related to decreased food intake and protein metabolism. Morphological changes in the heart tissue could not be appreciated. Venoruton (HR), administered at the dose of 300 mg/kg p.o. daily for 28 days (5 days before and 23 days after the first injection of adriamycin), improved adriamycin-induced clinical signs and symptoms (loss of body weight, hypothermia and decreased general vitality). It tended to increase cardiac output and stroke volume.

    Topics: Animals; Blood Chemical Analysis; Body Weight; Cardiac Output; Doxorubicin; Hemodynamics; Hydroxyethylrutoside; Male; Myocardium; Rats; Rats, Inbred Strains; Regional Blood Flow; Rutin

1985
Toxicity of venalot (a mixture of coumarin and troxerutin) in the baboon.
    Toxicology letters, 1983, Volume: 15, Issue:2-3

    Venalot, a mixture of coumarin and troxerutin, in the proportion 1 to 6 respectively, was given orally to baboons at dosages of 0, 100, 300 and 1000 mg/kg/day for 26 weeks. Vomiting, usually within 3 h of administration and considered to be of central origin, in addition to vomiting immediately after dosing, was noted in animals receiving 1000 mg/kg/day. At this level, collapse on several occasions in two animals, one of which died, was also observed. Another animal receiving 1000 mg/kg/day was killed for humane reasons following a period of weight loss, reduced appetite and deterioration in body condition. However, no adverse effect on body weight gain, food or water consumption, ophthalmoscopic or electrocardiographic examinations were noted in any other animals during this study. Increased levels of liver function (serum leucine amino-peptidase (LAP), and serum ornithine carbamyl transferase (OCT) were noted during the dosing period, together with slightly increased liver weights terminally for animals receiving 1000 mg/kg/day; however, as no morphological or ultrastructural changes were noted, these findings were considered to be attributable to hypertrophy.

    Topics: Animals; Body Weight; Coumarins; Drug Combinations; Female; Hydroxyethylrutoside; Liver; Male; Papio; Rutin; Vomiting

1983
[Reduction of radiation-induced early skin damage (mouse foot) by O-(beta-hydroxyethyl)-rutoside (author's transl)].
    RoFo : Fortschritte auf dem Gebiete der Rontgenstrahlen und der Nuklearmedizin, 1980, Volume: 133, Issue:3

    The effect of bioflavonoid, O-(beta-hydroxyethyl)-rutoside (HR) on early radiation-induced skin damage was examined, using the mouse foot system; the response to radiation is not species specific and comparison with the clinical situation is therefore possible. The aim was to see whether HR, which is highly effective in protecting against late damage, is also able to reduce early effects. Early reactions were considered to be erythema, swelling and ulceration and occurring up to 30 days after irradiation. It was found that HR significantly reduces early damage, both after a single dose and after fractionated irradiation with low doses. A single pre-treatment dose of HR and pre-treatment together with 30 days post-treatment administration were both found to be effective. The protective effect became more marked with increasing radiation dose (single irradiation). Reduction of late effects is produced optimally by an interval of 0.25 hours between application of HR and irradiation, and this is also true for early skin damage. The early effects are partly reversible, but there is possibly an interesting correlation between these and irreversible late effects (such as loss of toes); a similar mechanism, presumably affecting the vascular system, may therefore be postulated. The protective action of this well tolerated, highly effective substance, which apparently protects normal tissues from early and late injury, is discussed.

    Topics: Animals; Body Weight; Dose-Response Relationship, Drug; Dose-Response Relationship, Radiation; Foot; Hydroxyethylrutoside; Mice; Radiation Injuries; Radiation-Protective Agents; Rutin; Skin; Time Factors; Toes

1980