In vitro protective effect of Rhodiola rosea extract against hypochlorous acid-induced oxidative damage in human erythrocytes

Rhodiola rosea L. (Crassulaceae) is a plant living at high altitudes in Europe and Asia. Its roots have long been used in the traditional medical system of these geographical areas to increase the organism resistance to physical stress; today, it has become an important component of many dietary supplements. In this study we investigate the antioxidant capacity of the R. rosea aqueous extract evaluating its ability to counteract some of the main damages induced by hypochlorous acid (HOCl), a powerful oxidant generated by activated phagocytes, to human erythrocytes. Ascorbic acid was used as a reference substance because of its physiological HOCl-scavenging ability. Our study demonstrates that R. rosea is able to significantly protect, in a dose-dependent manner, human RBC from glutathione (GSH) depletion, glyceraldehyde-3-phosphate dehydrogenase (GAPDH) inactivation and hemolysis induced by the oxidant. Furthermore, we demonstrate that R. rosea aqueous extract acts from the inside of the erythrocyte suggesting a probable involving of cell components. The protection on GSH afforded by the R. rosea extract with respect to ascorbic acid, occurred also if added 2 or 5 min. later than the oxidant, suggesting a more rapid or powerful effect.     

The effect of desferrioxamine on peroxynitrite-induced oxidative damage in erythrocytes

The aim of this study was to investigate the effect of desferrioxamine on peroxynitrite-mediated damage in erythrocytes by measuring the 3-nitrotyrosine level and glutathione peroxidase and Na(+)-K(+) ATPase activities in vitro. 3-Nitrotyrosine levels were determined by HPLC; glutathione peroxidase and Na(+)-K(+) ATPase activities were measured by spectrophotometry. Peroxynitrite increased the 3-nitrotyrosine level but decreased both enzyme activities. In the presence of desferrioxamine, glutathione peroxidase activity was increased with a decrease in the 3-nitrotyrosine level. Desferrioxamine was found to possess an important antioxidant activity as assessed in an in vitro system, reducing protein nitration, restoring enzyme activities and maintaining erythrocyte membrane integrity.     

Black tea extract supplementation decreases oxidative damage in Jurkat T cells

The purpose of this study was to investigate the protective effect of black tea (BT) extract against induced oxidative damage in Jurkat T-cell line. Cells supplemented with 10 or 25 mg/L BT were subjected to oxidation with ferrous ions. Malondialdehyde (MDA) production as marker of lipid peroxidation, DNA single strand breaks as marker of DNA damage, and modification of the antioxidant enzyme activity, glutathione peroxidase (GPX) were measured. Results show the efficacy of BT polyphenols to decrease DNA oxidative damage and to affect GPX activity (P<0.05), while no effect was shown on MDA production. The succeeding investigation of the activity of caffeine and epigallocatechin gallate demonstrated their antioxidant potential with respect to the cellular markers evaluated. In conclusion, this study supports the protective effect of BT against ferrous ions induced oxidative damage to DNA and the ability of BT to affect the enzyme antioxidant system of Jurkat cells.     

In vitro studies on protective effect of Glycyrrhiza glabra root extracts against cadmium-induced genetic and oxidative damage in human lymphocytes

Cadmium is a modern environmental contaminant that is toxic and carcinogenic. Glycyrrhiza glabra is a traditional medicinal herb which grows in the various parts of the World. Recent studies demonstrated that G. glabra has antifungal, antimicrobial, antioxidant, and powerful antiinflammatory features. The purpose of this study was to investigate the genetic safety of extracts from G. glabra and its effects on cadmium (as CdCl₂) induced genotoxicity. Therefore we evaluated the capability of G. glabra extract to inhibit the rate of micronucleus (MN), sister chromatid exchange (SCE) formations induced by CdCl₂. Moreover, to assess the effects of G. glabra on cell viability and oxidative status, we performed 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) and total antioxidant capacity (TAC) assays. Our results showed that there were significant increases (P < 0.05) in both SCE and MN frequencies of cultures treated with CdCl₂ (5 ppm) as compared to controls. However, co-application of G. glabra extract (5, 10 and 20 ppm) and CdCl₂ resulted in decreases of MN and SCE rates as compared to the group treated with CdCl₂ alone. Again, the results of MTT and TAC assays clearly indicated dose dependent ameliorative effects of G. glabra extracts against CdCl₂ toxicity. In conclusion, this study demonstrated for the first time that G. glabra extracts provided increased resistance of DNA against CdCl₂ induced genetic and oxidative damage in human lymphocytes. So, the risk on target tissues of CdCl₂ could be reduced and ensured early recovery from its toxicity.     

叶黄素酯对四氧嘧啶所致小鼠氧化损伤的保护性研究

目的研究万寿菊花中提取的叶黄素酯体内对四氧嘧啶所致的小鼠氧化损伤的影响。方法采用分光光度法测定模型组肝组织超氧化物歧化酶（SOD）、丙二醛（MDA）、过氧化氢酶（CAT）、谷脱甘肽（GSH）、血清中天门冬氨酶氨基转移酶（AST）、丙氨酸氨基转移酶（ALT）、肝糖原,脑、心脏、股四头肌SOD、MDA的活性。结果叶黄素酯可抑制由于氧化损伤所致的小鼠肝SOD、MDA、CAT、GSH和血清中AST、AIJT的异常升高;降低脑、心脏、股四头肌SOD、MDA水平;降低血糖,提高肝糖元水平。结论叶黄素可通过影响组织、血清中相关酶活性而对四氧嘧啶所致的小鼠氧化损伤有一定的保护作用。     

Metformin does not prevent DNA damage in lymphocytes despite its antioxidant properties against cumene hydroperoxide-induced oxidative stress

Metformin (1-(diaminomethylidene)-3,3-dimethyl-guanidine), which is the most commonly prescribed oral antihyperglycaemic drug in the world, was reported to have several antioxidant properties such as the inhibition of advanced glycation end-products. In addition to its use in the treatment of diabetes, it has been suggested that metformin may be a promising anti-aging agent. The present work was aimed at assessing the possible protective effects of metformin against DNA-damage induction by oxidative stress in vitro. The effects of metformin were compared with those of N-acetylcysteine (NAC). For this purpose, peripheral blood lymphocytes from aged (n = 10) and young (n = 10) individuals were pre-incubated with various concentrations of metformin (10–50 μM), followed by incubation with 15 μM cumene hydroperoxide (CumOOH) for 48 h, under conditions of low oxidant level, which do not induce cell death. Protection against oxidative DNA damage was evaluated by use of the Comet assay and the cytokinesis-block micronucleus technique. Changes in the levels of malondialdehyde + 4-hydroxy-alkenals, an index of oxidative stress, were also measured in lymphocytes. At concentrations ranging from 10 μM to 50 μM, metformin did not protect the lymphocytes from DNA damage, while 50 μM NAC possessed an effective protective effect against CumOOH-induced DNA damage. Furthermore, NAC, but not metformin, inhibited DNA fragmentation induced by CumOOH. In contrast to the lack of protection against oxidative damage in lymphocyte cultures, metformin significantly protected the cells from lipid peroxidation in both age groups, although not as effective as NAC in preventing the peroxidative damage at the highest doses. Within the limitations of this study, the results indicate that pharmacological concentrations of metformin are unable to protect against DNA damage induced by a pro-oxidant stimulus in cultured human lymphocytes, despite its antioxidant properties.     

The protective effect of melatonin against cypermethrin-induced oxidative stress damage in Spodoptera litura (Lepidoptera: Noctuidae)

Antioxidant enzymes form the first-line defense against free radicals damage in organisms. Their regulation depends mainly on the oxidant and antioxidant status of the cell, given that oxidants are their principal modulators. Therefore, the aim of the present study was to investigate the effect of melatonin on synthetic pyrethroid insecticide-induced antioxidative enzymes activity in Spodoptera litura larvae. In addition, activities of enzymatic antioxidants viz. superoxide dismutase (SOD), glutathione S-transferase (GST), catalase (CAT), glutathione reductase (GR), α, β-esterase, and acetylcholine esterase (AChE) were assessed. There was no significant change in GST levels in the melatonin-treated groups. Melatonin modulates cypermethrin-induced changes in the activities of esterase and AChE, whereas SOD, CAT, and GR activity was significantly increased in melatonin-treated samples when compared to control. In conclusion, the results of the current study revealed that SP toxicity activated oxidant systems in all antioxidant systems in some tissues of insects. Melatonin administration led to a marked increase in antioxidant activity and inhibited GST and AChE in most of the tissues studied.     

Protective effect of lyophilized sapodilla (Manilkara zapota) fruit extract against CCl4-induced liver damage in rats

The tropical fruit sapodilla (Manilkara zapota syn. Achras zapota) is a rich source of nutrients, minerals and a myriad of bioactive phytochemicals such as flavonoids and catechins. Pharmacologically, sapodilla has been shown to exhibit anti-bacterial, anti-parasitic, anti-fungal, antiglycative, hypocholesterolemic and anti-cancer effects. However, its influence on hepatic tissue and serum lipids remains obscure. To address this, we used an in vivo model of liver damage to elucidate the effect of lyophilized sapodilla extract (LSE) treatment in carbon tetra chloride (CCl₄) intoxicated rats. Exposure of CCl₄ resulted in elevation of serum biomarkers of liver damage (aspartate transaminase, alanine aminotransferase, γ-glutamyl transferase and alkaline phosphatase), bilirubin and dysregulation of serum lipid profile (cholesterol and triglycerides). These effects were significantly and dose-dependently reversed by LSE treatment (250 and 500 mg/kg). Administration of LSE also reduced the structural damage caused by CCl₄ in the liver. Furthermore, determination of oxidative stress parameters (malondialdehyde and non-protein sulfhydryls) revealed that LSE treatment mitigated CCl₄-triggered modulation of both molecules. LSE also showed a strong antioxidant activity in 2,2-diphenyl-1-picrylhydrazyl (DPPH) and β-carotene-linoleic acid assays. In conclusion, the present study discloses the hepatoprotective and lipid-lowering effects of lyophilized sapodilla extract against CCl₄-induced liver damage, an effect, at least in part, mediated by its antioxidant activity.     

Olive leaf extract modulates permethrin induced genetic and oxidative damage in rats

Permethrin is a common synthetic chemical, widely used as an insecticide in agriculture and other domestic applications. The previous reports indicated that permethrin is a highly toxic synthetic pyrethroid pesticide to human and environmental health. Therefore, the present experiment was undertaken to determine the effectiveness of olive leaf extract in modulating the permethrin induced genotoxic and oxidative damage in rats. The animals used were broadly divided into four (A, B, C and D) experimental groups. Group A rats served as control animals and received distilled water intraperitoneally (n = 5). Groups B and C rats received intraperitoneal injections of permethrin (60 mg kg⁻¹ b.w) and olive leaf extract (500 mg kg⁻¹ b.w), respectively. Group D rats received permethrin (60 mg kg⁻¹ b.w) plus olive leaf extract (500 mg kg⁻¹ b.w). Rats were orally administered their respective feed daily for 21 days. At the end of the experiment rats were anesthetized and serum and bone marrow cell samples were obtained. Genotoxic damage was assessed by micronucleus and chromosomal aberration assays. Total antioxidant capacity and total oxidant status were also measured in serum samples to assess oxidative status. Treatment of Group B with permethrin resulted in genotoxic damage and increased total oxidant status levels. Permethrin treatment also significantly decreased (P < 0.05) total antioxidant capacity level when compared to Group A rats. Group C rats showed significant increases (P < 0.05) in total antioxidant capacity level and no alterations in cytogenetic parameters. Moreover, simultaneous treatments with olive leaf extract significantly modulated the toxic effects of permethrin in Group D rats. It can be concluded that olive leaf extract has beneficial influences and could be able to antagonize permethrin toxicity. As a result, this investigation clearly revealed the protective role of olive leaf extract against the genetic and oxidative damage by permethrin in vivo for the first time.     

Gastroprotective action of Cissus quadrangularis extract against NSAID induced gastric ulcer: role of proinflammatory cytokines and oxidative damage

The objective of this research was to analyse the gastroprotective effect of Cissus quadrangularis extract (CQE) along with its mechanism underlying the therapeutic action against the gastric mucosal damage induced by aspirin. In this study, we investigated the effect of CQE on the course of experimentally induced gastric ulcer by analyzing the levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), microvascular permeability, activity of nitric oxide synthase-2 (NOS-2), mitochondrial antioxidants, lipid peroxidation and DNA damage. A significant increase in vascular permeability, NOS-2 activity, TNF-alpha, IL-1beta levels and oxidative damage were noted in aspirin administered rats. Pretreatment with CQE (500 mg/kg bw/day) by oral gavage for 7 days significantly attenuated these biochemical changes caused by aspirin in rats. Tissue damage was showed by decreased levels of glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) and an associated rise in lipid peroxidation (LPO) in mitochondria, which were reversed by CQE. In addition, CQE prevents oxidative damage of DNA by reducing DNA fragmentation indicating its block on cell death. Ulcer protection in CQE treated rats was confirmed by histoarchitecture, which was comprised of reduced size of ulcer crater and restoration of mucosal epithelium. Thus, reduced neutrophil infiltration, antiapoptotic and antioxidant action have a pivotal role in the gastroprotective effect of CQE.     

Protective effect of Piper betle leaf extract against cadmium-induced oxidative stress and hepatic dysfunction in rats

The present study was undertaken to examine the attenuative effect of Piper betle leaf extract (PBE) against cadmium (Cd) induced oxidative hepatic dysfunction in the liver of rats. Pre-oral supplementation of PBE (200 mg/kg BW) treated rats showed the protective efficacy against Cd induced hepatic oxidative stress. Oral administration of Cd (5 mg/kg BW) for four weeks to rats significantly (P > 0.05) elevated the level of serum hepatic markers such as serum aspartate transaminase (AST), serum alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), gamma-glutamyl transpeptidase (GGT), bilirubin (TBRNs), oxidative stress markers viz., thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH), protein carbonyls (PC) and conjugated dienes (CD) and significantly (P > 0.05) reduced the enzymatic antioxidants viz., superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST), glutathione reductase (GR) and glucose-6-phosphate dehydrogenase (G6PD) and non-enzymatic antioxidants Viz., reduced glutathione (GSH), total sulfhydryls (TSH), vitamin C and vitamin E in the liver. Pre-oral supplementation of PBE (200 mg/kg BW) in Cd intoxicated rats, the altered biochemical indices and pathological changes were recovered significantly (P > 0.05) which showed ameliorative effect of PBE against Cd induced hepatic oxidative stress. From the above findings, we suggested that the pre-administration of P. betle leaf extract exhibited remarkable protective effects against cadmium-induced oxidative hepatic injury in rats.     

Protective role of Punica granatum L. peel extract against oxidative damage in experimental diabetic rats

Punica granatum L. (Punicaceae) peels extract had the highest free radical scavenging capacity among the tested medicinal plants which are being used traditionally for treatment of diabetes in Jordan. Accordingly, the present study aimed to investigate the antioxidant effect of P. granatum peel methanolic extract against oxidative damage in streptozotocin-induced diabetic rats. The antioxidant activity of P. granatum peel extract was investigated by examining the level of antioxidant enzymes, catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and glutathione reductase (GR), the serum total antioxidant capacity and lipid peroxidation in the tissues of treated diabetic rates comparing with normal and untreated diabetic ones. The results revealed that intraperitoneal administration of 10 and 20 mg kg⁻¹ (body weight) of P. granatum peel extract for 4 weeks significantly enhanced the activities of antioxidant enzymes in liver, kidney and RBC of STZ-induced diabetic rats. The extract also caused a significant reduction in malondialdehyde (MDA), a lipid peroxide's marker, in diabetic rat tissues and elevated the total serum antioxidant capacity in dose-dependent manner. In conclusion, this study clearly showed that P. granatum peel extract has protective role against the oxidative damage in STZ-induced diabetic rats.     

Effects of anesthetic alcohols on membrane transport processes in human erythrocytes

1. 1. Anesthetic alcohols (pentanol, hexanol and heptanol) were found to increase the fluidity of red cell membrane lipids as monitored by the fluorescence depolarization of diphenylhexatriene. The relative potency of the alcohols was found to be parallel to their relative membrane/water partition coefficients.

2. 2. Hexanol had biphasic effect on erythritol uptake by simple diffusion by red cells. At concentrations less than 9 mM, hexanol had no significant effect. At concentrations greater than 9 mM, there was an approximately linear increase in erythritol permeability with increasing alcohol concentration.

3. 3. The facilitated transport of uridine was markedly inhibited by hexanol. Hexanol at 6 mM produced a 65% inhibition of uridine (4 mM) uptake. Hexanol decreased both the apparent K_m and V values for the equilibrium exchange of uridine.

4. 4. The facilitated transport of galactose was only slightly inhibited by hexanol.

5. 5. Hexanol was without effect on the passive and active fluxes of Na⁺ and K⁺ in red cells with altered cation contents. Cells that were slightly depleted of K⁺ and cells that were highly K⁺-depleted were both insensitive to hexanol.

Antioxidative activity and protective effect of probiotics against high-fat diet-induced sperm damage in rats

In this study, antioxidant capability and protective effect of probiotics on reproductive damage induced by diet oxidative stress were investigated. Thirty male Sprague-Dawley rats were randomly divided into three groups with 10 rats in each group. The control group consumed a normal standard diet (5% fat, w/w). The other two treatment groups were fed with a high-fat diet (20% fat, w/w), and a high-fat diet supplemented with 2% probiotics (w/w), respectively. At the end of the experimental period, that is, after 6 weeks, rats were killed. Activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), contents of nitric oxide (NO) free radical and malondialdehyde (MDA) in serum and sperm suspension were examined. Sperm parameters including sperm concentration, viability, motility and DNA integrity were analyzed. The results showed that high-fat diet could induce oxidative stress, shown as significant increases in lipid peroxidation, NO free radical, significant decrease in activities of SOD, GSH-Px, significant reduction in sperm concentration, viability and motility, and damage in sperm DNA (P < 0.05), compared with the control group. These alterations were significantly reversed in the probiotics-supplemented group and had no significant difference in antioxidant capability, lipid peroxidation and sperm parameters compared with the control group. The percentage of sperm with DNA damage was significantly lower than the high-fat diet group and still higher than the control group, which means that probiotics could attenuate sperm damage to some extent. The present results indicated that dietary probiotics had antioxidant activity and the protective effect against sperm damage induced by high-fat diet to some extent.     

Nitric oxide protects against polyethylene glycol-induced oxidative damage in two ecotypes of reed suspension cultures

Dune reed (DR) is the more tolerant ecotype of reed to environmental stresses than swamp reed (SR). Under osmotic stress mediated by polyethylene glycol (PEG-6000), the suspension culture of SR showed higher ion leakage, and more oxidative damage to the membrane lipids and proteins was observed compared with the relatively tolerant DR suspension culture. Treatment with sodium nitroprusside (SNP) can significantly alleviated PEG-induced ion leakage, thiobarbituric acid reactive substances (TBARS) and carbonyl contents increase in SR suspension culture. The levels of H(2)O(2) and O(2)(-) were reduced, and the activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT) and ascorbate peroxidase (APX) were increased in both suspension cultures in the presence of SNP under osmotic stress, but lipoxygenase (LOX) activity was inhibited. 2-(4-carboxy-2-phenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO), a specific Nitric oxide (NO) scavenger, blocked the SNP-mediated protection. Depletion of endogenous NO with PTIO strongly enhanced oxidative damage in DR compared with that of PEG treatment alone, whereas had no effect on SR. Moreover, NO production increased significantly in DR while kept stable in SR under osmotic stress. Taken together, these results suggest that PEG induced NO release in DR but not SR can effectively protect against oxidative damage and confer an increased tolerance to osmotic stress in DR suspension culture.     

Hepatoprotective effect of bis(4‐methylbenzoyl) diselenide against CCl4‐induced oxidative damage in mice

From a pharmacological point of view, organoseleniums are compounds with important and interesting antioxidant and biological activities. The aim of this study was to evaluate the hepatoprotective effect of bis(4‐methylbenzoyl) diselenide (BMD) against carbon tetrachloride (CCl₄)–induced oxidative damage in mice. The animals received BMD (25 mg/kg p.o., for 3 days), and after 1 day, CCl₄ (1 mg/kg body weight) was administered by intraperitoneal route. One day after the CCl₄ exposure, the animals were euthanized for biochemical and histological analysis. Treatment with BMD (25 mg/kg p.o.) protected against aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma‐glutamyl transferase and lactate dehydrogenase activity increases induced by CCl₄ plasma exposure. Treatment with BMD (25 mg/kg) protected against increases in thiobarbituric reactive species and decreasing non‐protein thiols and ascorbic acid levels in liver of mice. Catalase and superoxide dismutase activity inhibition in the liver caused by CCl₄ were protected by treatment with BMD (25 mg/kg). Glutathione S‐transferase activity was inhibited by CCl₄ and remained unaltered even after treatment with BMD. Sections of liver from CCl₄‐exposed mice presented an intense infiltration of inflammatory cells and loss of the cellular architecture. BMD (25 mg/kg) attenuated CCl₄‐induced hepatic histological alterations. The results demonstrated the hepatoprotective effects of BMD in the mouse liver, possibly by modulating the antioxidant status. Copyright © 2012 John Wiley & Sons, Ltd.     

Xanthoria elegans (Link) (lichen) extract counteracts DNA damage and oxidative stress of mitomycin C in human lymphocytes

Several lichen species have been used for medicinal purposes throughout the ages, and they are reported to be effective in the treatment of different disorders including ulcer and cancer. It is revealed that lichens may be easily accessible sources of natural drugs and possible food supplements after their safety evaluations. The main objective in this study was to evaluate the roles of aqueous extracts of Xanthoria elegans (at 25, 50 and 100 μg/ml) upon mitomycin C (MMC; at 10⁻⁷ M) induced genotoxic and oxidative damages in cultured human lymphocytes. X. elegans were collected from the Erzurum and Artvin provinces (in Turkey) during August 2010. After the application of MMC and X. elegans extract (XEE), separate and together, human whole blood cultures were assessed by four genotoxicity end-points including chromosomal aberration, micronucleus, sister chromatid exchange (SCE) and 8-oxo-2-deoxyguanosine (8-OH-dG) assays. In addition, biochemical parameters [total antioxidant capacity (TAC) and total oxidative stress (TOS)] were examined to determine oxidative effects. According to our results, the frequencies of cytogenetic endpoints and 8-OH-dG levels were significantly increased by MMC compared with controls in human peripheral lymphocytes. MMC caused oxidative stress by altering TAC and TOS levels. On the contrary, XEE led to increases of TAC level without changing TOS level. XEE had no genotoxic effect. Furthermore, our findings revealed that MMC induced increases in the mean frequencies of four genotoxic indices were diminished by XEE in dose dependent manner, indicating its protective role towards cells from MMC exerted injury. In conclusion, the results obtained in the present study indicate for the first time that XEE is a potential source of natural antigenotoxicants.     

Purple carrot extract protects against cadmium intoxication in multiple organs of rats: Genotoxicity,oxidative stress and tissue morphology analyses

The aim of this study was to investigate if purple carrot extract is able to protect against the noxious activities induced by cadmium exposure in multiple organs of rats. For this purpose, histopathological analysis, genotoxicity and oxidative status were investigated in this setting. A total of twenty Wistar rats weighing 250 g on the average, and 8 weeks age were distributed into four groups (n = 5), as follows: Control group (non-treated group, CTRL); Cadmium group (Cd) and Purple carrot extract groups at 400 mg/L or 800 mg/L. Histopathological analysis revealed that liver from animals treated with purple carrot extract improved tissue degeneration induced by cadmium intoxication. Genetic damage was reduced in blood and hepatocytes as depicted by comet and micronucleus assays in animals treated with purple carrot extract. SOD-CuZn and cytocrome C gene expression increased in groups treated with purple carrot extract. Purple carrot extract also reduced the 8OHdG levels in liver cells when compared to cadmium group. Taken together, our results demonstrate that purple carrot extract is able to protect against cadmium intoxication by means of reducing tissue regeneration, genotoxicity and oxidative stress in multiple organs of Wistar rats.     

Experimental study of changes in osteoblastic shape induced by calcitonin and parathyroid extract in an organ culture system

Summary Neonate rat endocranial osteoblasts were cultured on their bone surfaces in control medium (CC) or medium to which either parathyroid extract (PTE) or calcitonin (CT) had been added for 2, 4, 8 or 24 h. Some were cultured for 24 h in CC, then for 2, 4, 8 or 24 h in either CT or PTE medium; or for 24 h in PTE, then for 2, 4, 8 or 24 h in either CC or CT; or 24 h in CT and 2, 4, 8 or 24 h in CC. The dorsal ruffling of the cells in CC was found to be suppressed by later culturing with PTE and the disoriented cells reorganized to form arrays of parallel cells. The effects of PTE were also reversed by CC or CT: the osteoblasts in the second culture (CC) lost elongation and order, and proceeded through a proliferative phase before exhibiting the ruffling form similar to a single CC 24 h culture. PTE-cultured osteoblasts showed an increase in cell overlap and contact so that a more competent barrier was formed separating the bone from the medium. In control or CT medium, however, intercellular gaps were greater than in vivo.We are grateful for the expert technical assistance of Elaine Bailey, for laboratory facilities kindly provided by Dr. Martin Evans, and for financial support from the Medical Research Council