Effect of n-Butanol on Chromosomal Damage in Mice Bone Marrow Cells

Background: n-Butanol is a four-carbon alcohol used widely in foods, cosmetics industries, biology and chemistry research laboratories, and other fields. Long time-effects of inhalation or consumption of small amounts of Butanol on human health are still unknown. On the other hand, numerous reports about the development of n-Butanol toxicity are available. The main objective of the study was to investigate the effects of inhaled and oral administration of n-Butanol as a long-term in vivo investigation.Materials and Methods: Small white laboratory, male mice (20-30 g) were used in 11 groups (n=4) including experimental 1 to 6, 1 to 4 control "A” and positive control groups. Experimental groups 1-3, for 10, 20, and 40 days; 5 hours a day were inside a box with ventilation facilities exposed to air saturated with n-Butanol vapor. Experimental groups 4 to 6, received water containing n-Butanol 0.2%, 1% and 5% for 10 days. Control groups B, 1 to 3 was placed for 10, 20, and 40 days inside a similar box exposed to normal air, respectively. Control group B 4 received water without any particular substance for 10 days. The positive control group received 30µl subcutaneous vinblastine. Bone marrow cells were extracted 24 hours after treatments and stained by May-Grünwald-Giemsa staining and the number of micronucleus was counted. Vinblastine, as a positive control, increased an average of micronucleus numbers significantly compared to control group (P<0.001).Results: n-Butanol inhalation caused no significant difference in 1-3 experimental groups in the average numbers of micronucleus compared to control group, even in the 40 days treatment group, average numbers of micronucleus was decreased comparing to control group (P<0.05). Also, oral administration of 0.2% and 1% n-Butanol had no effect on the average micronucleus numbers compared to the control group, while oral administration of 5% n-Butanol caused even decrease in average numbers of micronucleus compared to control group (P<0.05).Conclusion: n-Butanol inhalation may not cause chromosome damages in rat bone marrow cells that probably is due to its very fast metabolism and decomposition in the body. Therefore, the amount of n-Butanol in the systemic circulation and tissues is very low and, probably, the damaging potential is decreased

Effects of lead on the development of Drosophila melanogaster

Background and Purpose: Lead as a heavy metal and environmental pollutant causes sperm abnormalities, organogenesis, morphogenesis disorders and miscarriage. There are some similarities between mammals and Drosophila melanogaster. The present study is to investigate the lead-ion effects on some developmental aspects of Drosophila as a model. Materials and Methods: Five pairs of three-day flies were added to the culture containing different concentrations of lead-ion to mate and lay eggs. Transformation rate of larvae to pupa, pupa to adult, the required time for insect development and morphometric changes as well as eggs hatching rate for insects that developed in culture containing lead-ion were studied. Results: Culture-medium lead-ion (20-300 mg/L) increased larvae and pupae periods, but decreased the conversion rate of larvae to pupa, pupa to adult and eggs hatching. It also decreased the growth rate of larvae length/ width, pupa length/width and adult length. The results show that eggs length/width did not change. Conclusion: Factors such as the lead-ion interference with enzymes performances were involved in metamorphosis, reducing the mitochondrial cristae and ATP synthesis. In addition, the negative effect of lead on the production of growth hormones, metabolic enzymes and genes expression are the suggesting aspects for future study

Effects of Intrathecal Carbenoxolone Treatment on Nociception and Analgesia in Rat

Background: Gap junctions (GJ) are important in pain signalling at the spinal cord level. Aims: The aim of this investigation was to study the effects of GJ on nociception and the analgesic/hyperalgesic effects of mor­phine following administration of carbenoxolone as a GJ blocker. Male Wistar rats (200-250 g) were divided into three groups: saline i.p., 10 mg/kg and 1 μg/kg i.p. morphine, each with two subgroups. One was treated intrathecally with saline and the other with carben­oxolone. Study Design: Animal experiment. Methods: The thermal nociception threshold was measured prior to and after injections using the tail flick test. Chemical nociception assessment was conducted using a 0.05-mL subplantar injection of 2.5% formalin. Results: Both formalin-induced neurogenic and inflammatory nociception were reduced in the [saline i.p./carbenoxolone i.t.] and [morphine 1 µg/kg, i.p./carbenoxolone i.t.] subgroups (p<0.001). The 10 mg/kg i.p. morphine, i.t./carbenoxolone treatment reduced morphine-induced analgesia in the inflammatory phase (p<0.05), while it was ineffective in the neurogenic phase. Carbenoxolone decreased 1 µg/kg i.p. morphine-induced hyperalgesia in the tail flick test (p<0.001). Conclusion: Based on the results, GJ probably play a role in nociception at the spinal cord level. This may be due to the facilitation of inflammatory mediators released from glial cells or the connection between stimulatory interneurons and projection neurons. GJ blocking attenuated morphine-induced analgesia. This may be due to the attenuation of pre/post-synaptic inhibitory effects of morphine at the spinal cord level. As demonstrated by the investigations, GJ are present between inhibitory interneurons. Therefore, we can assume that blockage of GJ between inhibitory interneurons will reduce morphine-induced analgesia at the spinal cord level. However, this requires further investigation

Role of C-fibers during acute and chronic stress on formalin-induced paw edema in rats

633-637Stimulation of peripheral nociceptors leads to releasing of some mediators such as substance P (SP) and Calcitonin gene-related peptide (CGRP) and contributes to the edema formation by vasodilatation induction. On the other hand glucocorticoids have anti-inflammatory action, and they are elevated in the plasma during stress. This communication reports C-fibers inflammatory role and the effects of chronic and acute stress and/or dexamethasone (as stress mimicry) on paw edema induced by formalin at presence/deficit C-fibers rats. Acute stress and dexamethasone and chronic dexamethasone have shown an anti-inflammatory effect in C-normal groups, but chronic stress had no effect on inflammation. C-fibers reduction (C-lesion) had anti-inflammatory effects. In deficit C-fibers rats, acute and chronic stress had not stronger anti-inflammatory effect, but acute dexamethasone reduced the anti-inflammatory effect of C-fibers reduction while in the same condition, chronic dexamethasone induced stronger anti-inflammatory effect. The results show C-fiber nerve produce and release the peripheral inflammatory mediators, "C-fibers reduction" decreased the paw inflammation. Counter adaptation in C-lesion animals may reduce the modulatory effects of dexamethasone on the remaining C-fibers. Acute dexamethasone diminished the "C-fibers reduction" anti-inflammatory effect, but at chronic treatment, the modulatory effects of dexamethasone aggregated and it augmented the C-fibers reduction anti-inflammatory effect

The effect of Ferula szowitsiana extract on chemical pain in male Wistar rats

Investigations on the use of medicinal plants are appealing to researchers. In Iranian traditional medicine, Ferula szowitsiana is used as an analgesic. This study investigates the effect of the extract of aerial parts of Ferula szowitsiana on an experimental model of chemical pain induced by subplantar injection of formalin. The Ferula szowitsiana hydroalcoholic extract was prepared with ethanol, Tween 80 and saline at a ratio of 8:1:1 serving as a solvent. Wistar Rats in the weight range of 200-250 g were divided into 10 groups randomly (n=7) according to treatment applied as follows: control; solvent (intraperitoneal, i.p.); solvent (intrathecal, i.t.); extract (50, 100, 200, 400 mg/kg i.p.); extract (80 μg/10 μL i.t); naloxone (2 mg/kg i.p.); extract (400 mg/kg) and naloxone (i.p.). To study the chemical pain, subplantar administration of formalin was performed in all groups. The results showed that the extract could reduce chemical pain in the neurogenic and inflammatory phase dose dependently as compared to the control group. The magnitude of the response after intrathecal administration of a dose of 80 μg/10μL was comparable to that observed with 400 mg/kg of extract administered via the intraperitoneal route. The administration of naloxone as an opioid receptor antagonist reversed the analgesic effect of the extract completely. According to the results, it seems that at least a significant part of the analgesic effect of Ferula szowitsiana extract is exerted through its effect on the central nervous system, and the analgesic effect of the extract in acute and inflammatory chemical pain is due to its effect on the opioid system

Neuroprotective Effects of Exercise on Brain Edema and Neurological Movement Disorders Following the Cerebral Ischemia and Reperfusion in Rats

Introduction: Cerebral ischemia and reperfusion causes physiological and biochemical changes in the neuronal cells that will eventually lead to cell damage. Evidence indicates that exercise reduces the ischemia and reperfusion-induced brain damages in animal models of stroke. In the present study, the effect of exercise preconditioning on brain edema and neurological movement disorders following the cerebral ischemia and reperfusion in rats was investigated. Methods: Twenty-one adult male wistar rats (weighing 260-300 g) were randomly divided into three groups: sham operated, exercise plus ischemia, and ischemia group (7 rats per group). The rats in exercise group were trained to run on a treadmill 5 days a week for 4 weeks. Transient focal cerebral ischemia and reperfusion were induced by middle cerebral artery occlusion (MCAO) for 60 minutes, followed by reperfusion for 23 hours. After 24 hours ischemia, movement disorders were tested by a special neurological examination. Also, cerebral edema was assessed by determining the brain water content. Results: The results showed that pre-ischemic exercise significantly reduced brain edema (P<0.05). In addition, exercise preconditioning decreased the neurological movement disorders caused by brain ischemia and reperfusion (P<0.05). Conclusion: Preconditioning by exercise had neuroprotective effects against brain ischemia and reperfusion-induced edema and movement disorders. Thus, it could be considered as a usefulstrategy for prevention of ischemic injuries, especially in people at risk

Effects of repeated anesthesia by thiopental in neonatal period on PTZ-induced convulsions and pain responses during maturation in rats

Introduction: General anesthetics during critical periods of brain development may cause some seriousmalformations or side effects. Anesthetic drugs can involve in the brain development and synaptogenesis atthe critical period of development. There are some controversy with regards the effects of(neurodegenerative or neuroprotective) barbiturates on brain. The aim of the present study was toinvestigate the possible relation between repeated induced thiopental (a GABAA agonist) anesthesia at thepostnatal period and pentylentetrazol-induced convulsions and pain responses in adult in the Wistar rats.Materials and methods: 40 male neonate rats were divided into experimental and sham groups. Theexperimental group (n=20) was deeply anesthetized with thiopental (30 mg/kg daily) during 10 to 20-daysof post- natal period and physiologic serum was used for sham animals. After maturation of male rats, thePTZ-induced seizures were induced by daily interapritoneally injection of PTZ (45 mg/kg), and thelatency of the appearance of generalized epileptiform behaviors was recorded. Pain responses were alsoevaluated using tail-flick and formalin tests.Results: No significant differences were found in the lantency of the appearance of behaviouralconvulsions and pain sensitivity between experimental and sham groups.Conclusion: Our findings indicate that prior exposure to thiopental during nenonatal stage has no effectson PTZ-induced seizures and also pain responses after maturation. Developmental compensatorymechanisms may protect the brian against the possible damage that induced by repeated thipopental duringneonatal period

Neuroprotective Effects of Exercise on Brain Edema and Neurological Movement Disorders Following the Cerebral Ischemia and Reperfusion in Rats

Introduction: Cerebral ischemia and reperfusion causes physiological and biochemical changes in the neuronal cells that will eventually lead to cell damage. Evidence indicates that exercise reduces the ischemia and reperfusion-induced brain damages in animal models of stroke. In the present study, the effect of exercise preconditioning on brain edema and neurological movement disorders following the cerebral ischemia and reperfusion in rats was investigated. Methods: Twenty-one adult male wistar rats (weighing 260-300 g) were randomly divided into three groups: sham operated, exercise plus ischemia, and ischemia group (7 rats per group). The rats in exercise group were trained to run on a treadmill 5 days a week for 4 weeks. Transient focal cerebral ischemia and reperfusion were induced by middle cerebral artery occlusion (MCAO) for 60 minutes, followed by reperfusion for 23 hours. After 24 hours ischemia, movement disorders were tested by a special neurological examination. Also, cerebral edema was assessed by determining the brain water content. Results: The results showed that pre-ischemic exercise significantly reduced brain edema (P<0.05). In addition, exercise preconditioning decreased the neurological movement disorders caused by brain ischemia and reperfusion (P<0.05). Conclusion: Preconditioning by exercise had neuroprotective effects against brain ischemia and reperfusion-induced edema and movement disorders. Thus, it could be considered as a usefulstrategy for prevention of ischemic injuries, especially in people at risk

Involvement of Vanilloid Receptors in the Anti-inflammatory Effect of Hydroalcoholic Extract of Heated Female Cannabis sativa Flowers in Rat

Background and Objectives: Decarboxylated phytocannabinoids activate endocannabinoid system in the central nervous system and peripheral tissues via activation of cannabinoid receptors. In this investigation, the effect of interaction between decarboxylated phytocannabinoids and capsaicin at the central level and naloxone at the systemic level, was investigated on inflammatory rat paw edema induced by by sub-plantar injection. Methods: In this experimental study, male Wistar rats (200-250g) were used. To study the effect of interaction with opioid system, intraperitoneal administration of hydroalcoholic extract (dose, 50mg/kg), naloxone (dose, 2mg/kg) and co-administration of the extract and naloxone were performed. To investigate the effect of interaction with vanilloid system, intrathecal administration of extract (0.01mg/10&mu;l), capsaicin (0.002mg/10&mu;l) and co-administration of extract and capsaicin were performed. Paw volume was measured before and one hour after sub-plantar administration of formalin using plethysmometer method in order to assess inflammatory edema. Results: Intraperitoneal administration of extract alone or in combination with naloxone reduced the inflammatory rat paw edema volume (p<0.001). On the other hand, capsaicin increased rat paw edema volume (p<0.01), but intrathecal administration of extract alone and in combination with capsaicin decreased the inflammatory rat paw edema volume (p<0.01). Conclusion: The results of this study showed that decarboxylated cannabinoids in hydroalcoholic extract decrease the capsaicin-induced inflammatory rat paw edema through activation of CB1 and CB2 receptors and desensitization of TRPV1 receptor. On the contrary, administration of naloxone has not antagonized the reduction effect of extract on inflammatory paw edema, and it is likely that the effect of the extract has not exerted through opioid receptors