Protective effect of safranal against hexachlorobutadiene-induced nephrotoxicity in rat

Hexachlorobutadiene [HCBD] is a potent nephrotoxin in rodents, which can cause degeneration, necrosis and regeneration in renal tubular epithelial cells. It has been shown that safranal, the active ingredient of saffron, has a protective effect against ischemic injuries. The aim of this study was to examine the protective effect of safranal against HCBD-induced nephrotoxicity in rats. Method: Thirty Wistar albino rats were randomly divided in five groups. The rats received a single dose of corn oil 1ml/kg [group1], HCBD 50mg/kg [group 2], or safranal at doses of 0.5, 0.25 and 0.1 ml/kg one hour before HCBD [50mg/kg] injection [groups 3-5]. All injections were carried out intraperitoneally. Urine samples were collected one day before, and one day after injections. On day 3 the animals were sacrificed and both kidneys were removed. The right kidney was fixed in formalin for histological examination and the left kidney was homogenized for measuring malondialdehyde [MDA]. Blood samples were taken by cardiac puncture and used for the measurement of urea, creatinine, glucose and protein concentrations. Blood urea concentration in HCBD treated group was significantly higher compared with group 3 [p<0.01] and groups 1 and 4 [p<0.001]. There was no significant difference in urea concen-trations between group 5 and HCBD treated group. Urinary concentration of glucose was significantly higher in group 2, compared with groups 1, 3 and 4 [p<0.001] No significant differences were observed in urinary glucose concentrations between HCBD- and safranal [0.1ml/kg]-treated groups. Concentration of protein was also significantly higher in group 5 than those of other tested groups [p<0.001]. Safranal at doses of 0.25 and 0.5ml/kg has a protective effect against HCBD-induced nephrotoxicity in rats

[Lectin histochemical method for the dectection of surface sugars in the adrenal medullary cells of embryos and newborn mice]

To distinguish the special effect of terminal sugar/sugars on development of adrenal gland medulla fetal or afterbirth. Determining the days that they are effective on development as inductive factors was another objective. In the study, we used of 12 females and 4 males BALB/c mice. Fetuses of all gestational days and newboms up to 15 days of age were fixed and processed by common histological techniques, and sections were obtained from adrenal region. The number of normal newborns and embryos were 78 heads. To distinguish the terminal sugars, we used lectins that are PNA [peanut agglutinin], VVA [vicia villosa agglutinin] and GSA1-B4 [griffonia simplia-B4]. Lectins were detected by DAB [diaminobenzidin] dye after binding to terminal sugars. Adrenal medulla cells reacted only to PNA at 13th gestational day to birth and up to 15[th] after birth. Several sections from all of specimens which we used for the lectin histochemistery study did not react to three other lectins. Findings of this study elucidated that Gal-GalNAc terminal sugar, which is specific to PNA lectin, is a key terminal sugar in studied days. So we suggest that Gal-GalNAc has a key role on adrenal medulla development at 13[th] fetal day to birth and 15 days afterbirth

[Effect of safranal, a constituent of saffron [Crocus sativus L.], on lipid perioxidation level during renal ischemia - reperfusion injury in rats]

Generation of reactive oxygen species and lipid peroxidation are associated with tissue injury following ischemic insult. It has been shown that saffron extract has antitumor, chemopreventive and radical scavenger properties as well as protective effects on genotoxins-induced oxidative stress and promote the diffusivity of oxygen in different tissues. The aim of the present study was to assess the effect of safranal, a constituent of saffron [Crocus sativus L.], on lipid peroxidation level and histopatological alterations following renal ischernia-reperfusion injury [IRI] in rats. In order to induct renal ischemia-reperfusion injury, the left kidney was exposed to warm ischemia for 60 min followed by reperfusion for 90 min. Safranal [with doses of 0.1 ml/kg, 0.25 ml/kg-gand 0.5 ml/kg, i.p.] and normal saline [10 ml/kg, i.p.] were administrated prior to induction of ischemia. The lipid peroxidation level [which expressed as thiobarbituric acid reactive species, TBARS] and histopatological alteration were evaluated in kidney of control and ischemic groups. Ischemia-reperfusion injury [IRI] caused a significant increase in TBARS levels [from 119.7 to 379.2 nmol/g tissue, p<0.001].In safranal pretreated groups, a significant reduction in TBARS levels [from 379.2 to 110.6 nmol/g tissue, p<0.001;0.5 ml/kg], as compared with control group, was observed. Histopathological data also showed that safranal attenuated renal ischemiareperfusion injury. This study, therefore, suggests that safranal may be a useful agent for the prevention of lipid peroxidation following renal ischemia-reperfusion injury [IRI] in rats

histopathological changes of mice liver due to morphine administration

Morphine is an opioid analgesic and has known effects on different organs. This study was done to determine the histopatological; changes of liver due to morphine administration in adult mice. In this experimental study, 20 male Blab/c mice divided experiment and control groups. In experiment and control group, animals received 15mg/kg/day morphine and salin normal interperitoneally, for 2days respectively. Day 22 the livers were dissected under anesthesiology. Specimens were processed for histological study and stanied with H and E. In experimental group, small sites of necrosis with poly morphic inflammatory infiltration and debris formation of necrotized nucleus in death area, so hepatitis was suggested. Also accumulation of micro droplets of lipid inside the hepatocyte cytoplasm withont nucleus displacement [fatty damages with small vacuoles] observed in cases. In addition, microvesicular steatosis and mouth teeth necrosis in liver parenchyma with inflammation in the vein and portal space were seen in cases. Any changes was not seen in control group. The interperitoneal administration of morphine can cause histopatological changes in mice liver

Protective effect of calcium channel blockers against hexachlorobutadienenephrotoxicity in rat

Hexachlorobutadiene [HCBD] is a potent nephrotoxine in rodents. Its toxicity is due to its conjugation by glutathione [GSH] to form glutathione s-conjugate, by the enzyme glutathione S-transferase, and finally to the related cysteine-conjugate. This metabolite is then actively taken up by kidney and cleared in the renal tubular epithelial cells to a reactive thiol derivative, by the enzyme [3-lyase that covalently binds to the macromolecules. There are several studies regarding the protective effects of calcium channel blockers against some nephrotoxicants. Also our previous study showed that verapamil is able to protect the kidney against HCBD; therefore, in this study the protective effect of diltiazem and nifedipin [calcium blockers] against HCBD-induced nephrotoxicity in rat was examined.In this study, W/A rats from either sex were divided in 6 groups. Group one dosed with corn oil [1 ml/kg, i/p], group two dosed with HCBD [50mg/kg, i.p], and groups 3 to 6 dosed with [50 and/or 100microg/kg, i.p] diltiazem and nifedipine one hour before HCBD [50mg/kg] as single dose. After 24 hours, all animals were killed; blood samples were taken by cardiac puncture for measuring urea and creatinin. The kidneys were removed and fixed in formalin for histopathologic examination,. Concentration of urea as a marker of kidney damage, in group two [66.3 +/- 15.3mg/dl] was significantly higher than all other groups [33.8 +/- 3.2, 29.3 +/- 8.1, 29.3 +/- 9.2, 26.5±4, 33.8 +/- 3.8mg/dl] for control and groups 3-6 respectively. Also concentration of creatinin in group two [1.08 +/- 0.3 mg/dl] was significantly higher than all other groups [0.53 +/- 0.05, 0.57 +/- 0.06, 0.57 +/- 0.06, 0.53 +/- 0.05, 0.53 +/- 0.05mg/dl] for control and groups 3-6 respectively. Microscopic studies showed that there was substantial necrosis in the straight portion of the proximal tubules in HCBD-treated group. In the calcium-blocker treated groups, the renal proximal tubules showed a normal appearance and no damage were observed. In conclusion, diltiazem and nifedipine are able to protect the kidney against toxic effect of HCBD in rat

[Distribution of Galactose-N Acetyl Galactoseamine on the surface of adult mice kidney cells]

Background and Objective: carbohydrate chains link to glycoproteins and glycolipids of the cell surface particulary their terminal sugars have key roles in cellular activities of almost all biological systems. Distribution of these glycoconjugates in adult kidney has not received fair attention yet. The purpose of this study was to identify in situ location of galactose - N - acetyle galactoseamine moleucles on the surface of the adult rat kidney

Materials and Methods: after the resection of rat kidney and rotin fixation with regular lectin histochemical technique, MPA and PNA conjugated to horseradish peroxidase, lectins specific to indentify these terminal sugars in rat kidney

Results: intense reaction of PNA to collective tubules, less intense and reaction with luminal surface of proximal tubules and MPA identified distinct cells among distal tubules as well as glomerules were observed

Conclusion: it seems that this specific sugars related to the cellulars function of this region of adult kidney and probably genetically is regulated during embryonic development