scholarly journals Chronic exposure to quinalphos shows biochemical changes and genotoxicty in erythrocytes of silver barb, Barbonymus gonionotus

2017 ◽  
Vol 10 (3) ◽  
pp. 99-106 ◽  
Author(s):  
Islam M. Sadiqul ◽  
Saimon Mohiful Kabir ◽  
Zannatul Ferdous ◽  
Khan Mst. Mansura ◽  
Rahman Md. Khalilur
Keyword(s):  
Freshwater Fish ◽  
Chronic Exposure ◽  
Genotoxic Effects ◽  
Nuclear Abnormalities ◽  
Biochemical Characteristics ◽  
Lipid Contents ◽  
Dose Dependent ◽  
Lethal Doses ◽  
Silver Barb

AbstractAnin vivostudy was carried out on the freshwater fishBarbonymus gonionotusto evaluate the genotoxic effects of the organophosphate quinalphos. The fish were exposed to sub-lethal doses of quinalphos (0%, 10%, 25%, and 50% of LC50) for a period of 30 days. Analysis of biochemical characteristics (protein and lipid contents of different organs), nuclear abnormalities of erythrocytes (NAE) and morphological abnormalities of erythrocytes (MAE) were performed on peripheral erythrocytes sampled at post-treatment intervals of 0 and 30 days. The biochemical results revealed a significant dose-dependent decline in protein and lipid contents and increase in the frequencies of NAE as well as MAE. Our findings also confirmed that the morphological deformations of erythrocytes in addition to NAE on fish erythrocytesin vivoare effective tools in determining the potential genotoxicity of organophosphates.

In vivo protection studies of bis-quaternary 2-(hydroxyimino)-N-(pyridin-3-yl) acetamide derivatives against sarin poisoning in mice

2016 ◽  
Vol 36 (1) ◽  
pp. 23-32 ◽  
Author(s):  
Devyani Swami ◽  
Hitendra N Karade ◽  
Jyotiranjan Acharya ◽  
Pravin Kumar
Keyword(s):  
Time Course ◽  
Lethal Dose ◽  
Nerve Agent ◽  
Ache Inhibition ◽  
Inhibition Concentration ◽  
Time Course Study ◽  
Dose Dependent ◽  
Protection Index ◽  
Lethal Doses

In vivo antidotal efficacy of new bis- quaternary 2-(hydroxyimino)- N-(pyridin-3yl) acetamide derivatives (HNK series), to counter multiples of lethal doses of nerve agent sarin (GB) and reactivation of acetylcholinesterase (AChE), was evaluated in Swiss albino mice. [Protection index PI; median lethal dose (LD50) of sarin with treatment/LD50 of sarin] was estimated, using 0.05, 0.10, and 0.20 LD50 as treatment doses of all the oximes with atropine against sarin poisoning. Dose-dependent time course study was conducted at 0.2, 0.4 and 0.8 LD50 dose of sarin for estimating maximum AChE inhibition. At optimized time (15 min), in vivo enzyme half inhibition concentration (IC50) was calculated. AChE reactivation efficacy of HNK series and pralidoxime (2-PAM) were determined by plotting shift of log IC50 doses. HNK-102 with atropine showed three fold higher PI compared to 2-PAM. In vivo IC50 of sarin for brain and serum AChE was found to be 0.87 LD50 (139.2 µg/kg) and 0.48 LD50 (77.23 µg/kg), respectively. Treatment with HNK-102 and HNK-111 (equal to their 0.20LD50) significantly reactivated sarin-intoxicated AChE ( p < 0.05) at 2× IC50 dose of sarin, compared to 2-PAM. The study revealed that HNK-102 oxime was three times more potent as antidote, for acute sarin poisoning compared to 2-PAM in vivo.

Protein phosphatase inhibition and in vivo hepatotoxicity of microcystins

1993 ◽  
Vol 265 (2) ◽  
pp. G224-G230 ◽  
Author(s):  
M. T. Runnegar ◽  
S. Kong ◽  
N. Berndt
Keyword(s):  
Protein Phosphatase ◽  
Intraperitoneal Injection ◽  
Significant Inhibition ◽  
Protein Phosphatase 1 ◽  
Liver Protein ◽  
Protein Phosphatase Inhibition ◽  
Clinical Changes ◽  
Dose Dependent ◽  
Lethal Doses

Administration of microcystin (MCYST)-YM or -LR (peptide hepatotoxins produced by the cyanobacterium Microcystis aeruginosa) to mice resulted in the inhibition of liver protein phosphatase 1 and 2A activity. In all cases significant inhibition preceded or accompanied clinical changes due to MCYST intoxication. Fifteen minutes after intraperitoneal injection of lethal doses of MCYST-YM protein phosphatase activity was already decreased to 44% of controls, and by 60 min was further decreased to 22% of controls. The inhibition was dose dependent: intraperitoneal injection with 84 nmol/kg of MCYST-YM and 48 nmol/kg of MCYST-LR were the minimum doses required for significant inhibition at 60 min. Pretreatment of mice with 200 mumol/kg of rifamycin prevented the inhibition of liver protein phosphatase. The inhibition was tissue specific, with none detected in the kidneys, an organ that, unlike the liver, does not accumulate MCYST. In contrast to MCYST intoxication, lethal doses of phalloidin, a peptide hepatotoxin that produces clinical and pathological changes similar to MCYST, did not cause any inhibition of protein phosphatases.

scholarly journals APPLICABILITY OF THE AMES TEST AND MICRONUCLEUS TEST IN VIVO FOR THE EVALUATION OF THE EQUIVALENCE OF PESTICIDE TECHNICAL GRADE ACTIVE INGREDIENTS COMPARED TO ORIGINAL ACTIVE SUBSTANCES

2019 ◽  
Vol 98 (2) ◽  
pp. 219-224
Author(s):  
Nataliya A. Ilyushina ◽  
O. V. Egorova ◽  
Yu. A. Revazova
Keyword(s):  
Ames Test ◽  
Mouse Bone Marrow ◽  
Active Ingredients ◽  
Genotoxic Effects ◽  
Technical Grade ◽  
Technical Products ◽  
Dose Dependent ◽  
Active Substances

Introduction. Analogs of pesticides may differ from the original products in their properties because of the elevated level or the modified composition of the impurities. Therefore, it is necessary to determine the equivalence of such analogs using a number of criteria, including mutagenicity, to ensure their safety. The article compares the results of the research of genotoxic effects of technical grade active ingredients of pesticides in vitro and in vivo conditions to assess the applicability of such methods for equivalence determination of analogs of pesticides to patented products. Material and methods. The genotoxicity of 99 technical grade active ingredients of pesticides (59 names) was studied in vitro (Ames test) and in vivo. Results. In the Ames test mutagenic dose-dependent effects were revealed in the study of technical products of mesotrione, dimethoate, and pendimethalin both in the presence and in the absence of a metabolic activation system.In the in vivo test, a statistically significant dose-dependent increase in the frequency of micronucleated polychromatophilic erythrocytes in mouse bone marrow was detected after administration of six technical products mesotrione, pyrimiphos-methyl, dimethoate, glyphosate (2 products), isoproturon. Furthermore, different levels of genotoxic effects were found with technical materials of the same active ingredient from various productions, probably due to differences in the qualitative and quantitative composition of impurities. Conclusion. The present study indicated that in vitro and in vivo tests do not always demonstrate the same results of the genotoxicity assessment. Therefore, the use of only one bacterial reverse mutation test may not be sufficient to determine the equivalence of technical grade active ingredients of pesticides to the original active substances. To obtain а reliable evidence for the safe use of analogs of pesticides, it is necessary to usе at least two methods on different test objects.

scholarly journals Cytotoxic and genotoxic effects of perfluorododecanoic acid (PFDoA) in Japanese medaka

2018 ◽  
pp. 9
Author(s):  
Isaac O Ayanda ◽  
Min Yang ◽  
Zhang Yu ◽  
Jinmiao Zha
Keyword(s):  
Dna Damage ◽  
Comet Assay ◽  
Chronic Exposure ◽  
Tail Length ◽  
Toxicity Study ◽  
Japanese Medaka ◽  
Genotoxic Effects ◽  
Gradual Decline ◽  
Nuclear Abnormalities ◽  
Fish Blood

This study investigated the cytotoxic and genotoxic potential of perfluorododecanoic acid (PFDoA), a perfluorinated carboxylic chemical (PFC) that has broad applications and distribution in the environment in Japanese medaka, Oryzias latipes. Micronucleus (MN) test and Comet assay were used for the toxicity study. Three groups of fish were exposed to 0.1 mg/L, 0.5 mg/L and 2.5 mg/L concentration of the chemical for 28 days. Another group served as control. Sampling of the fish blood and liver were done after days 1, 4, 7, 14, 21 and 28 for analysis of different erythrocyte abnormalities and damage to DNA using the MN test and Comet assay respectively. Results showed that there was a significant time and concentration dependent increase (p < 0.05) in percent tail length of DNA and frequency of erythrocyte abnormalities. Nuclear abnormalities observed include micronucleus, fragmented apoptotic cells, lobed nuclei, and bean-shaped cells. Increase in induction of erythrocyte abnormalities and percent tail length of DNA peaked at days 14 and 7, respectively, after which there was a gradual decline. The results indicate that sub-chronic exposure of PFDoA to Japanese medaka caused DNA damage with a simultaneous induction of different erythrocyte abnormalities.

In vivo and in vitro exposures for the evaluation of the genotoxic effects of lead on the Neotropical freshwater fish Prochilodus lineatus

2011 ◽  
Vol 104 (3-4) ◽  
pp. 291-298 ◽  
Author(s):  
V. Monteiro ◽  
D.G.S.M. Cavalcante ◽  
M.B.F.A. Viléla ◽  
S.H. Sofia ◽  
C.B.R. Martinez
Keyword(s):  
Freshwater Fish ◽  
Genotoxic Effects ◽  
Prochilodus Lineatus

Involvement of 5-Hydroxytryptamine in Platelet Aggregation In Vivo in Rats and Guinea Pigs

1989 ◽  
Vol 61 (03) ◽  
pp. 463-467 ◽  
Author(s):  
G M Smith
Keyword(s):  
Platelet Count ◽  
Guinea Pigs ◽  
Platelet Adhesion ◽  
Adenosine Diphosphate ◽  
Rate Of Return ◽  
Low Doses ◽  
Dose Dependent ◽  
Higher Doses ◽  
Rat Platelets

SummaryIn this study, 5-hydroxytryptamine (5-HT) caused a dose- dependent fall in the circulating platelet count suggesting that 5-HT receptors are activated in rat platelets to cause platelet adhesion and aggregation. When low doses of adenosine diphosphate (ADP) were simultaneously injected with 5-HT, there was a significant potentiation of the responses to ADR Ketanserin significantly reduced the potentiated responses. When higher doses of ADP were infused with bolus injections of 5-HT there was no potentiation and ketanserin did not reduce these responses. Ketanserin did not inhibit the collagen-induced fall in circulating platelet count, but did significantly increase the rate of return to the basal platelet count compared with control. 5-HT did not cause a fall in platelet count in guinea-pigs

Effects of NO-Donors on Thrombus Formation and Microcirculation in Cerebral Vessels of the Rat

1996 ◽  
Vol 76 (01) ◽  
pp. 111-117 ◽  
Author(s):  
Yasuto Sasaki ◽  
Junji Seki ◽  
John C Giddings ◽  
Junichiro Yamamoto
Keyword(s):  
Blood Flow ◽  
Thrombus Formation ◽  
Dependent Manner ◽  
Red Cell ◽  
Cell Velocity ◽  
Red Cell Velocity ◽  
The Mean ◽  
Wall Shear ◽  
Dose Dependent

SummarySodium nitroprusside (SNP) and 3-morpholinosydnonimine (SIN-1), are known to liberate nitric oxide (NO). In this study the effects of SNP and SIN-1 on thrombus formation in rat cerebral arterioles and venules in vivo were assessed using a helium-neon (He-Ne) laser. SNP infused at doses from 10 Μg/kg/h significantly inhibited thrombus formation in a dose dependent manner. This inhibition of thrombus formation was suppressed by methylene blue. SIN-1 at a dose of 100 Μg/kg/h also demonstrated a significant antithrombotic effect. Moreover, treatment with SNP increased vessel diameter in a dose dependent manner and enhanced the mean red cell velocity measured with a fiber-optic laser-Doppler anemometer microscope (FLDAM). Blood flow, calculated from the mean red cell velocity and vessel diameters was increased significantly during infusion. In contrast, mean wall shear rates in the arterioles and venules were not changed by SNP infusion. The results indicated that SNP and SIN-1 possessed potent antithrombotic activities, whilst SNP increased cerebral blood flow without changing wall shear rate. The findings suggest that the NO released by SNP and SIN-1 may be beneficial for the treatment and protection of cerebral infarction

Soluble Thrombomodulin Purified from Human Urine Exhibits a Potent Anticoagulant Effect In Vitro and In Vivo

1995 ◽  
Vol 73 (05) ◽  
pp. 805-811 ◽  
Author(s):  
Yasuo Takahashi ◽  
Yoshitaka Hosaka ◽  
Hiromi Niina ◽  
Katsuaki Nagasawa ◽  
Masaaki Naotsuka ◽  
...  
Keyword(s):  
Human Urine ◽  
Specific Activity ◽  
Anticoagulant Activity ◽  
Rabbit Lung ◽  
Soluble Thrombomodulin ◽  
Molecular Weights ◽  
Dose Dependent Fashion ◽  
Dose Dependent

SummaryWe examined the anticoagulant activity of two major molecules of soluble thrombomodulin purified from human urine. The apparent molecular weights of these urinary thrombomodulins (UTMs) were 72,000 and 79,000, respectively. Both UTMs showed more potent cofactor activity for protein C activation [specific activity >5,000 thrombomodulin units (TMU)/mg] than human placental thrombomodulin (2,180 TMU/mg) and rabbit lung thrombomodulin (1,980 TMU/mg). The UTMs prolonged thrombin-induced fibrinogen clotting time (>1 TMU/ml), APTT (>5 TMU/ml), TT (>5 TMU/ml) and PT (>40 TMU/ml) in a dose-dependent fashion. These effects appeared in the concentration range of soluble thrombomodulins present in human plasma and urine. In the rat DIC model induced by thromboplastin, administration of UTMs by infusion (300-3,000 TMU/kg) restored the hematological abnormalities derived from DIC in a dose-dependent fashion. These results demonstrate that UTMs exhibit potent anticoagulant and antithrombotic activities, and could play a physiologically important role in microcirculation.

Adenosine Diphosphate (ADP)-Induced ⍺-Granules Release from Platelets of Native Whole Blood Is Reduced by Ticlopidine but Not by Aspirin or Dipyridamole

1986 ◽  
Vol 56 (02) ◽  
pp. 147-150 ◽  
Author(s):  
V Pengo ◽  
M Boschello ◽  
A Marzari ◽  
M Baca ◽  
L Schivazappa ◽  
...  
Keyword(s):  
Whole Blood ◽  
Light Transmission ◽  
Ex Vivo ◽  
Early Stage ◽  
Shape Change ◽  
Adenosine Diphosphate ◽  
Dose Dependent ◽  
Plateletderived Growth Factor ◽  
Platelet Shape

SummaryA brief contact between native whole blood and ADP promotes a dose-dependent release of platelet a-granules without a fall in the platelet number. We assessed the “ex vivo” effect of three widely used antiplatelet drugs, aspirin dipyridamole and ticlopidine, on this system. Aspirin (a single 800 mg dose) and dipyridamole (300 mg/die for four days) had no effect, while ticlopidine (500 mg/die for four days) significantly reduced the a-granules release for an ADP stimulation of 0.4 (p <0.02), 1.2 (p <0.01) and 2 pM (p <0.01). No drug, however, completeley inhibits this early stage of platelet activation. The platelet release of α-granules may be related to platelet shape change of the light transmission aggregometer and may be important “in vivo” by enhancing platelet adhesiveness and by liberating the plateletderived growth factor.

Glial cytotoxicity of low doses of cadmium as a model of heavy metal pollution influence on vertebrates

2020 ◽  
Vol 31 (1) ◽  
pp. 3-10
Author(s):  
V. S. Nedzvetsky ◽  
V. Ya. Gasso ◽  
A. M. Hahut ◽  
I. A. Hasso
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Oxidative Damage ◽  
Cadmium Chloride ◽  
Glioma Cells ◽  
Low Doses ◽  
Genotoxic Effects ◽  
Cadmium Ions

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p <0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p <0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.

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