Decrease In Tail Length Research Articles

Potential therapeutic effect of synthesized AgNP using curcumin extract on CCl4-induced nephrotoxicity in male mice

Nephrotoxicity is a particularly important challenge in a clinical context. Oxidative stress, plays an important role in the pathogenesis of kidney. Curcumin has a potential antioxidant impacts, despite of its low water solubility and bioavailability which restricts its uptake. Here, we elevated curcumin solubilization and bioactivity by including in a modified silver nanoparticles. This study is aimed at assessing the protective impacts of silver nanoparticles with curcumin (AgNP-curcumin) against CCl4-induced injury in mice kidney. C57BL/6 mice were categorized into three groups. Group 1 mice received vehicle only. Group 2 mice received a single dose of 1 mL/kg CCl4 in paraffin. Group 3 mice were treated with 2.5 mg/kg AgNP-curcumin twice a week for 3 weeks after receiving CCl4 challenge. Results showed that CCl4 disrupted oxidative markers. Reduced glutathione was significantly decreased and the lipid peroxidation indicator MDA was significantly elevated in the CCl4 group. Urea, creatinine and gamma glutamyl transferase (GGT) were significantly elevated in the CCl4 group. However, lactate dehydrogenase (LDH) was significantly decreased. Severe histopathological changes were observed in the renal tissues in the CCl4 group compared with the findings in the control group. AgNP-curcumin was found to significantly restore the oxidative balance and kidney structure and function. The comet assay showed that CCl4 increases nuclear DNA tail length (DNA damage) by 76.36% compared with the control, while AgNP-curcumin demonstrated a decrease in tail length by 30.53% relative to that in the CCl4 group. Through its antioxidant activity, AgNP-curcumin showed a potential role in preventing the deleterious effects of CCl4 on DNA in renal tissues.

Morphological adjustment in free-living Steinernema feltiae infective juveniles to increasing concentration of Nemafric-BL phytonematicide.

Third-stage larvae (L3) of Steinernema feltiae exist as free-living infective juveniles (IJ), with suspended development activities. In contrast, parasitic stages (L1, L2, L4, adult) have mutualistic relations with Xenorhabdus species bacteria, along with unique morphological changes and development inside the cadaver of host insects and/or plant-parasitic nematodes. Commercial IJ strains are tolerant to cucurbitacin-containing phytonematicides, but we have scant information on how morphological adjustments in IJ are achieved. In this study, we investigated the nature of morphological adjustments in commercial S. feltiae IJ strains to Nemafric-BL phytonematicide, which contains cucurbitacin B as active ingredient. Post-72 h exposure to phytonematicide concentration, IJ specimens were fixed on mounting slides. Length (body, excretory pore to anterior end, pharynx, rectum, stoma, tail), diameter (head width, neck base, mid-body, anal body), cuticle thickness and De Man ratios were measured with a computer software programme attached to Omax light microscope. Morphometric data against increasing phytonematicide concentration exhibited either density-dependent quadratic, linear or neutral relations. Increase in body length at low phytonematicide concentration was accompanied by decrease in tail length and pharynx length during muscle contraction when IJ were still alive. After death at high phytonematicide concentration, the opposite morphometric effects ensued due to muscle relaxation. The observed changes in morphometric structures were explained on the basis of morphological adjustments that modulated volumes of pseudocoelom cavity in IJ. The modulation is intended to maintain hydrostatic pressure within permissible upper limits in order to avoid structural damage to internal organs embedded in the pseudocoelom fluids.

Evaluation of Mango Byproduct Extracts as Antioxidant against Pb-acetate induced Oxidative Stress and Genotoxicity in Mice

The antioxidant and antiproliferative properties of mango by-products were investigated. This study was carried out to evaluate the protective role of mango peel or kernel defatted extracts against Pb-acetate adverse effects on oxidant/antioxidant status, liver dysfunction biomarkers, histopathological changes and genotoxicity in male mice. Total phenolic content and antioxidant activity of both extracts were evaluated. Two doses of both extracts (50 and 100 mg/kg) were used to evaluate their role against the toxicity of Pb-acetate (500 ppm). Mice given mango extracts with Pb-acetate had signifi cantly lower plasma MDA, AST and ALT and higher glutathione than mice given Pb-acetate alone. Mango extracts prevented the histopathological changes in liver induced by Pb-acetate and decreased the cytotoxicity of lead by increasing the ratio of PCE/NCE. Mango extract treatment reduced the DNA damage induced by Pb-acetate in liver as demonstrated by a reduction in micronuclei and decrease in tail length, tail DNA% and Olive tail moment. It can be concluded that mango by-product extracts have potential to protect from oxidative stress and genotoxicity of lead.

Amelioration of 5-FU induced toxicity by using RF under white light: An in vitro study

Fluorouracil (5-FU) is a potent photosensitizer used in colon and rectal cancer. A major drawback associated with 5-FU chemotherapy is its toxicity towards normal tissues by generation of reactive oxygen species (ROS). Riboflavin (RF) is a well known photosensitizer and has no adverse effect. Previously, we have reported the ameliorative effect of photoilluminated RF in case of cisplatin induced toxicity both in vitro and in vivo. Accordingly, we have extended our work and have tried to demonstrate with the help of carbonyl assay that the rise in the carbonyl groups reached a certain level at particular concentration of 5-FU and after which no increase in oxidative damage of protein was observed. However, on addition of RF in the reaction the photo excitation of 5-FU was inhibited at lower concentration. Moreover, plasmid nicking also elucidate that the nicking activity is minimally affected by the incorporation of 5-FU at higher concentration in the reaction and on addition of RF at lower concentration of 5-FU the nicking of plasmid was masked. Furthermore, on incubation of lymphocytes with lower concentration of 5-FU in presence of RF as compared to 5-FU alone led to a significant decrease in tail length of DNA when measured by comet assay. Thus, study show that 5-FU behaves in a biphasic manner, at lower concentrations of the drug in which RF inhibits the photoactivation leading to quenching in the ROS generation while at higher concentration the drug dimerization is thought to be the plausible reason for the observed results. In conclusion, our results suggest that 5-FU induced toxicity may be blunted by using RF under white light.

Quantifying the effect of feather abrasion on wing and tail lengths measurements

Wing and tail length measurements are important tools in ornithology. Amongst linear measurements, wing length has been considered to be the best indicator for body size for taxonomy and ecomorphology, as well as for studies about the impact of climate change on morphology. As feathers are dead tissue, abrasion will lead to a reduction in wing and tail length within a moult cycle. The aim of our study was to analyse the effect of feather abrasion on wing and tail length in the Stonechat Saxicola torquata. Generalized additive models revealed that wing lengths and tail lengths decrease significantly between the termination of feather growth and the next moult. The decrease in wing length was faster with increasing feather age. The decrease in tail length was nearly linear through time. Multiple measurements of recaptured individuals revealed a similar decrease in wing length to that observed in analyses based on single measurements of multiple individuals. An analysis of the length of the third outermost primary revealed the same pattern. Hence, the decrease in wing and tail length over time was caused by within-bird changes and not by mortality, emigration or immigration associated with wing and tail length. We found that feather abrasion was more pronounced in females compared to males at least during the breeding season, but there were no strong indications that feather abrasion was more pronounced in birds before their first complete moult compared to older individuals. A review of previous studies showed that a reduction in wing length of about 0.2–0.5 %/month is a common phenomenon. Our study shows that feather abrasion must be taken into account when analysing time-series of wing and tail length measurements to avoid spurious conclusions.

Potential protective effects of vitamin E on diazinon-induced DNA damage and some haematological and biochemical alterations in rats

Diazinon (DZN), is a commonly used organophosphorous (OP) pesticide to control a variety of insects in agriculture and in the environment. Vitamin E is a primary antioxidant that plays an important role in protecting cells against toxicity by inactivating free radicals generated following pesticides exposure. Therefore, the present study was undertaken to investi- gate the possible protective effect of vitamin E against DZN- induced adverse effects on haematological and biochemical indices and on genotoxicity using comet assay and micronucleus test for measuring the DNA damage. The tissue DZN residues in liver, kidney and muscle of the rats were determined. Vitamin E (200 mg/kg, twice a week), diazinon (10mg/kg/ day, once a day), and vitamin E (200mg/kg, twice a week + diazinon (10mg/kg/day, once a day) combination were given to rats (n= 10) orally via gavage for 4 weeks. The results revealed that DZN administration significantly decreased Hb concentration, RBCs count and PCV values. Meanwhile, a significant increased in WBCs, ALT, AST and total cholesterol was detected. However, vitamin E supplementation together with DZN improves these alterations. DZN residues level is highest in the kidney than that in liver and muscle tissues. Administration of vitamin E together with DZN reduces the residual values in the examined tissues. A significant increase in tail length of comets from blood cells as well in the fre- quency of micronucleated cells (MNCs) following DZN administration was achieved. Co-administrated vitamin E along with DZN resulted in decrease in tail length of comets and the percentage of MNCs compared to DZN alone treated rats. The increase in frequency of MNCs and tail length of comets confirm the genotoxicity of DZN. Vitamin E, on the other hand, was observed to repair the genotoxicity and improves the haematological and biochemical changes induced by DZN. It can be concluded that vitamin E has protective effect against DZN adverse effects and supplementation of vitamin E might be beneficial to DZN exposed populations.

Antisense Morpholino-mediated knockdown of type 3 iodothyronine deiodinase in the embryonic zebrafish (Danio rerio)

Event Abstract Back to Event Antisense Morpholino-mediated knockdown of type 3 iodothyronine deiodinase in the embryonic zebrafish (Danio rerio) Marjolein Heijlen1*, Camila V. Esguerra2, Alexander D. Crawford2 and Veerle M. Darras1 1 Catholic University of Leuven, Department of Biology, Faculty of Science, Belgium 2 Catholic University of Leuven, Department of Pharmaceutical Sciences, Faculty of Pharmaceutical Sciences, Belgium Although the pivotal role of thyroid hormones (THs) in vertebrate development has been widely documented, little information is available on their role in early embryogenesis. Early teleost embryos rely on the maternal TH deposit in the egg yolk, consisting predominantly of T4. In adult zebrafish, as in most other vertebrates, a tight control of intracellular T3 levels is achieved by the combined action of the three types of iodothyronine deiodinases (D1-D3). Recently, our team investigated the importance of the two Ds capable of T4 to T3 conversion, D1 and D2, during early embryogenesis in zebrafish. This research showed that D2 is the major contributor to TH activation in developing zebrafish embryos (1). We have now inhibited the expression of the TH inactivating enzyme, D3, by antisense morpholino-mediated knockdown. To estimate the impact of D3 knockdown on the rate of embryonic development, three morphological indices were measured: otic vesicle length, tail length and pigmentation index. The increase in otic vesicle length and the decrease in tail length and pigmentation index were all indicative of an aberrant development. Additional morphological abnormalities observed in some embryos were pericardial edema, flattening of the head, curved tail and an overall decrease in size. To control for a possible induction of a p53-dependent cell death pathway, which is the major off-targeting effect of morpholinos, we repeated the experiments with concurrent knockdown of p53. Since this did not rescue the phenotype, we can conclude that the observed defects are indeed D3-dependent. Our present results indicate that next to intracellular TH activation also local inactivation by D3 is essential for normal early development in zebrafish embryos. References (1) Walpita, C.N., A.D. Crawford, and V.M. Darras, Combined antisense knockdown of type 1 and type 2 iodothyronine deiodinases disrupts embryonic development in zebrafish (Danio rerio). Gen Comp Endocrinol, 2009. 166(1): p. 134-41. Keywords: comparative endocrinology Conference: 25th Conference of the European Comparative Endocrinologists, Pécs, Hungary, 31 Aug - 4 Sep, 2010. Presentation Type: Conference Presentation Topic: Comparative endocrinology Citation: Heijlen M, Esguerra CV, Crawford AD and Darras VM (2010). Antisense Morpholino-mediated knockdown of type 3 iodothyronine deiodinase in the embryonic zebrafish (Danio rerio). Front. Endocrinol. Conference Abstract: 25th Conference of the European Comparative Endocrinologists. doi: 10.3389/conf.fendo.2010.01.00030 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 26 Aug 2010; Published Online: 29 Aug 2010. * Correspondence: Miss. Marjolein Heijlen, Catholic University of Leuven, Department of Biology, Faculty of Science, Leuven, Belgium, marjolein.heijlen@bio.kuleuven.be Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Marjolein Heijlen Camila V Esguerra Alexander D Crawford Veerle M Darras Google Marjolein Heijlen Camila V Esguerra Alexander D Crawford Veerle M Darras Google Scholar Marjolein Heijlen Camila V Esguerra Alexander D Crawford Veerle M Darras PubMed Marjolein Heijlen Camila V Esguerra Alexander D Crawford Veerle M Darras Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Protective effects of vitamin E against atrazine-induced genotoxicity in rats

Atrazine (2-chloro-4-(ethylamino)-6-(isopropylamino)- s-triazine) is one of the most commonly used herbicides to control grasses and weeds. The widespread contamination and persistence of atrazine residues in the environment has resulted in human exposure. Vitamin E is a primary antioxidant that plays an important role in protecting cells against toxicity by inactivating free radicals generated following pesticides exposure. The present study was undertaken to investigate the protective effect of vitamin E against atrazine-induced genotoxicity. Three different methods: gel electrophoresis, comet assay and micronucleus test were used to assess the atrazine-induced genotoxicity and to evaluate the protective effects of vitamin E. Atrazine was administered to male rats at a dose of 300 mg/kg body weight for a period of 7, 14 and 21 days. There was a significant increase ( P < 0.001) in tail length of comets from blood and liver cells treated with atrazine as compared to controls. Co-administration of vitamin E (100 mg/kg body weight) along with atrazine resulted in decrease in tail length of comets as compared to the group treated with atrazine alone. Micronucleus assay revealed a significant increase ( P < 0.001) in the frequency of micronucleated cells (MNCs) following atrazine administration. In the animals administrated vitamin E along with atrazine there was a significant decrease in percentage of micronuclei as compared to atrazine treated rats. The increase in frequency of micronuclei in liver cells and tail length of comets confirm genotoxicity induced by atrazine in blood and liver cells. In addition, the findings clearly demonstrate protective effect of vitamin E in attenuating atrazine-induced DNA damage.

DNA damage in leukocytes of mice treated with copper sulfate

Single stranded DNA breaks induced by copper sulfate (CuSO4) in mice has been studied in vivo using Alkaline Single Cell Gel Electrophoresis (Comet assay). Mice were administered orally with doses of 0, 1.25, 2.50, 5.00, 7.50, 10.00 and 12.50 mg/kg body weight (b.wt.) of CuSO4 respectively. The samples of whole blood were collected at 24, 48, 72 h, first week and second week post-treatment and the assay was carried out to determine single strand DNA breaks as represented by comet tail-length. In addition, the sample was used to study the repair efficiency by incubating the samples with RPMI medium for 2 h. Results indicated a significant DNA damage at all the doses after treatment with CuSO4 when compared to controls showing a clear dose-dependent response (p<0.05). A gradual decrease in the tail-lengths from 48 h post-treatment was observed and by second week, the values returned to control levels at all doses. The study on the repair efficiency indicated that mice treated with all the doses of CuSO4 showed decrease in mean comet tail-length indicating repair efficiency capacity but less when compared to those of controls. The study also reveals that comet assay is a sensitive and rapid method for detecting DNA damage caused by trace metals such as copper (Cu).

Changes in specific prolactin binding in Rana catesbeiana tadpole tissues during metamorphosis and following prolactin and thyroid-hormone treatment

The prolactin-binding affinity ( K D ) and number of binding sites N in Rana catesbeiana tadpole, tail fin and kidney tissues were studied during metamorphosis and following administration of oPRL and L-T 3 to premetamorphic tadpoles. With increasing developmental stage there was an increase in N; a maximum was found at stage XVIII followed by a gradual decrease in N through metamorphic climax for all 3 tissues. No change in K d was noted. lL-T 3 treatment of premetamorphic tadpoles for 7 days caused a significant decrease in tail length and height and body length and an increase in hindlimb length with a concurrent increase in N of approximately 3-fold while treatment for 1 or 3 days was without effect on tadpole morphology or oPRL binding. oPRL treatment for 7 days caused a significant increase in tail length and height and body length with no significant changes in hindlimb length and a 3–5-fold increase in N. Treatment with both L-T 3 and oPRL for 7 days resulted in an inhibition of the T 3- induced decrease in tail length and height and body length and no inhibition of the hindlimb length increase. N increased in all tissues similar to that found with either treatment alone. No change in K D was noted in any of these studies. Therefore, oPRL and L-T 3 are able to regulate the numbers of specific oPRL-binding sites in amphibian tissues. The change in N with development parallels the reported change in tadpole pituitary capacity to stimulate growth but occurs prior to the reported surge of endogenous T 3 during metamorphosis. Thus, the variation in the number of oPRL-binding sites may be due to the changes in endogenous PRL levels during development.