Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome

2011 ◽  
Vol 14 (3) ◽  
pp. 443-448 ◽  
Author(s):  
N. Kurhalyuk ◽  
H. Tkachenko ◽  
K. Pałczyńska

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome In the present work we evaluated the effect of ulcerative dermal necrosis (UDN) syndrome on resistance of erythrocytes to haemolytic agents and lipid peroxidation level in the blood from brown trout (Salmo trutta m. trutta L.). Results showed that lipid peroxidation increased in erythrocytes, as evidenced by high thiobarbituric acid reactive substance (TBARS) levels. Compared to control group, the resistance of erythrocytes to haemolytic agents was significantly lower in UDN-positive fish. Besides, UDN increased the percent of hemolysated erythrocytes subjected to the hydrochloric acid, urea and hydrogen peroxide. Results showed that UDN led to an oxidative stress in erythrocytes able to induce enhanced lipid peroxidation level, as suggested by TBARS level and decrease of erythrocytes resistance to haemolytic agents.

2021 ◽  
Vol 18 ◽  
Author(s):  
Sobia Manzoor ◽  
Ayesha Khan ◽  
Beena Hasan ◽  
Shamim Mushtaq ◽  
Nikhat Ahmed

Background: Oxidative damage contributes to the pathophysiology of schizophrenia (SZ). Redox imbalance may lead to increased lipid peroxidation, which produces toxic aldehydes like 4-hydroxynonenal (4-HNE) ultimately leading to oxidative stress. Conversely, implications of oxidative stress points towards an alteration in HNE-protein adducts and activities of enzymatic and antioxidant systems in schizophrenia. Objectives: Present study focuses on identification of HNE-protein adducts and its related molecular consequences in schizophrenia pathology due to oxidative stress, particularly lipid peroxidation. Material and Methods: Oxyblotting was performed on seven autopsied brain samples each from cortex and hippocampus region of schizophrenia patients and their respective normal healthy controls. Additionally, thiobarbituric acid substances (TBARS), reduced glutathione (GSH) levels and catalase (CAT) activities associated with oxidative stress, were also estimated. Results: Obtained results indicates substantially higher levels of oxidative stress in schizophrenia patients than healthy control group represented by elevated expression of HNE-protein adducts. Interestingly, hippocampus region of schizophrenia brain shows increased HNE protein adducts compared to cortex. An increase in catalase activity (4.8876 ± 1.7123) whereas decrease in antioxidant GSH levels (0.213 ± 0.015µmol/ml) have been observed in SZ brain. Elevated TBARS level (0.3801 ± 0.0532ug/ml) were obtained in brain regions SZ patients compared with their controls that reflects an increased lipid peroxidation (LPO). Conclusion: Conclusion: We propose the role of HNE modified proteins possibly associated with the pathology of schizophrenia. Our data revealed increase lipid peroxidation as a consequence of increased TBARS production. Furthermore, altered cellular antioxidants pathways related to GSH and CAT also highlight the involvement of oxidative stress in schizophrenia pathology.


2008 ◽  
Vol 5 (1) ◽  
pp. 55-59 ◽  
Author(s):  
P. Chaturvedi

In the present study, inhibitory effect of the methanol extract ofRaphanus sativusroot on lipid peroxidation has been carried out in normal rats. Graded doses of methanol extract of root of the plant (40, 80 and 120 mg kg−1body weight) were administered orally for 15 days to experimental treated rats. Distilled water was administered to experimental control rats. At the end of experiment, rats were killed by decapitation after ether anesthesia. Blood and liver were collected to measure thiobarbituric acid reactive substance, reduced glutathione and activity of catalase. Results indicated that the extract ofR. sativusroot reduced the levels of thiobarbituric acid reactive substance significantly in all experimental treated groups (P < 0.05) as compared to the experimental control group. It also increased the levels of reduced glutathione and increased the activity of catalase.In vitroexperiments with the liver of experimental control and experimental treated rats were also carried out against cumene hydroperoxide induced lipid peroxidation. The extract inhibitedin vitrocumene hydroperoxide induced lipid peroxidation.R. sativusinhibits lipid peroxidationin vivoandin vitro. It provides protection by strengthening the antioxidants like glutathione and catalase. Inclusion of this plant in every day diet would be beneficial.


2002 ◽  
Vol 80 (3) ◽  
pp. 193-197 ◽  
Author(s):  
A C de Oliveira ◽  
V D'Almeida ◽  
D C Hipólide ◽  
J N Nobrega ◽  
S Tufik

Hyperhomocysteinemia has been associated with pathological and stressful conditions and is a risk factor for cardiovascular disease. Since sleep deprivation is a stressful condition that is associated with disruption of various physiological processes, we investigated whether it would also be associated with increases in plasma homocysteine levels. Further, since hyperhomocysteinemia may promote oxidative stress, and we had previously found evidence of oxidative stress in brain following sleep deprivation, we also searched for evidence of systemic oxidative stress by measuring glutathione and thiobarbituric acid reactive substance levels. Rats were sleep deprived for 96 h using the platform technique. A group was killed after sleep deprivation and another two groups were allowed to undergo sleep recovery for 24 or 48 h. Contrary to expectation, plasma homocysteine was reduced in sleep-deprived rats as compared with the control group and did not revert to normal levels after 24 or 48 h of sleep recovery. A trend was observed towards decreased glutathione and increased thiobarbituric acid reactive substance levels in sleep-deprived rats. It is possible that the observed decreases in homocysteine levels may represent a self-correcting response to depleted glutathione in sleep-deprived animals, which would contribute to the attenuation of the deleterious effects of sleep deprivation.Key words: sleep deprivation, homocysteine, oxidative stress, glutathione, rats.


2011 ◽  
Vol 64 (7-8) ◽  
pp. 377-380 ◽  
Author(s):  
Aleksandra Novakov-Mikic ◽  
Snezana Brkic ◽  
Daniela Maric ◽  
Bojan Sekulic ◽  
Aleksandar Cetkovic ◽  
...  

Pre-eclampsia is characterized by increased lipid peroxidation and diminished antioxidant capacity. The aim of the study was to establish concentration of thiobarbituric acid reactive substances as a marker of lipid peroxidation in normal pregnancies and in pregnancies complicated with pre-eclampsia, and to estimate the possibility of using thiobarbituric acid reactive substances as a screening method for development of pre-eclampsia. The study was conducted at the Department of Obstetrics and Gynaecology, Clinical Centre of Vojvodina. The study included 57 singleton pregnancies, gestation >24 weeks, of which 29 were healthy pregnancies and 28 were with pre-eclampsia, defined as systolic arterial pressure of >90 mmHg, diastolic of >145 mmHg, and 24h proteinuria of >300mg. Thiobarbituric acid reactive substances concentrations evaluated by malondialdehyde equivalent standards (OxiSelect? TBARS Assay Kit (malondialdehyde Quantitation), Cell Biolabs? OxiSelect?) showed that oxidative stress was more evident in the group with pre-eclampsia, though not statistically significant (p= 0.107). There was no correlation of thiobarbituric acid reactive substance levels with gestation in either group. The differences between the level of thiobarbituric acid reactive substance concentrations in pre-eclampsia and healthy pregnancies indicate the possibility of using thiobarbituric acid reactive substances as a screening tool for the development of pre-eclampsia. Further studies with larger numbers of patients are needed in order to come to final conclusions.


2019 ◽  
Vol 51 (06) ◽  
pp. 389-395 ◽  
Author(s):  
Gregorio Caimi ◽  
Baldassare Canino ◽  
Maria Montana ◽  
Caterina Urso ◽  
Vincenzo Calandrino ◽  
...  

AbstractThe association between obesity and cardiovascular diseases has a multifactorial pathogenesis, including the synthesis of inflammatory molecules, the increase in oxidative stress and the dysregulation of the matrix metalloprotease (MMP) concentration and activity. In a group of adults with obesity, divided in 2 subgroups according to the body mass index (BMI), we examined lipid peroxidation, expressed as thiobarbituric acid-reactive substances (TBARS), protein oxidation, expressed as protein carbonyl groups (PCs), plasma gelatinases (MMP-2 and MMP-9), and their tissue inhibitors (TIMP-1 and TIMP-2). In the whole group, as well as in the 2 subgroups (with BMI 30–35 or BMI>35) of obese subjects, we observed an increase in TBARS, PCs, MMP-2, and MMP-9, and also TIMP-1 and TIMP-2 in comparison with the control group. A positive correlation between TBARS and PCs emerged in obese subjects and persisted after dividing obese subjects according to BMI. The correlation between MMP-2 and TIMP-2 was not statistically significant, while a significant correlation was present between MMP-9 and TIMP-1. The correlations between the markers of oxidative stress (TBARS and PCs) and those of the MMP/TIMP profile indicated a more marked influence of protein oxidation on MMPs and TIMPs in comparison with TBARS. The innovative aspect of our study was the simultaneous evaluation of oxidative stress markers and MMP/TIMP profile in adult obese subjects. We observed significant alterations and correlations that may negatively influence the clinical course of the disease.


2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Krzysztof Jagiełło ◽  
Tomasz Zalewski ◽  
Stefan Dobosz ◽  
Oliwia Michalik ◽  
Konrad Ocalewicz

Mitotic gynogenesis results in the production of fully homozygous individuals in a single generation. Since inbred fish were found to exhibit an increased frequency of body deformations that may affect their survival, the main focus of this research was to evaluate the ratio of individuals with spinal deformities among gynogenetic doubled haploids (DHs) brown trout as compared to nonmanipulated heterozygous individuals. Gynogenetic development was induced by the activation of brown trout eggs by UV-irradiated homologous and heterologous (rainbow trout) spermatozoa. The subsequent exposure of the activated eggs to the high hydrostatic pressure disturbed the first cleavage in gynogenetic zygotes and enabled duplication of the maternal haploid set of chromosomes. The survival rate was significantly higher among gynogenetic brown trout hatched from eggs activated with the homologous UV-irradiated spermatozoa when compared to DHs hatched from eggs activated by the heterologous spermatozoa. More than 35% of the gynogenetic larvae exhibited body deformities, mostly lordosis and scoliosis. The percentage of malformed brown trout from the control group did not exceed 15%. The increased number of deformed larvae among DHs brown trout suggested rather a genetic background of the disease related to the fish spine deformities; however, both genetic and environmental factors were discussed as a cause of such conditions in fish.


Chemosphere ◽  
2006 ◽  
Vol 65 (10) ◽  
pp. 1707-1714 ◽  
Author(s):  
Bjørn Henrik Hansen ◽  
Svein Rømma ◽  
Liv I.R. Søfteland ◽  
Pål A. Olsvik ◽  
Rolf A. Andersen

Chemosphere ◽  
2007 ◽  
Vol 67 (11) ◽  
pp. 2241-2249 ◽  
Author(s):  
Bjørn Henrik Hansen ◽  
Svein Rømma ◽  
Øyvind Aaberg Garmo ◽  
Sindre Andre Pedersen ◽  
Pål Asgeir Olsvik ◽  
...  

2010 ◽  
Vol 299 (3) ◽  
pp. G661-G668 ◽  
Author(s):  
Courtney S. Schaffert ◽  
Michael J. Duryee ◽  
Robert G. Bennett ◽  
Amy L. DeVeney ◽  
Dean J. Tuma ◽  
...  

Ethanol metabolism in the liver induces oxidative stress and altered cytokine production preceding myofibroblast activation and fibrogenic responses. The purpose of this study was to determine how ethanol affects the fibrogenic response in precision-cut liver slices (PCLS). PCLS were obtained from chow-fed male Wistar rats (200–300 g) and were cultured up to 96 h in medium, 25 mM ethanol, or 25 mM ethanol and 0.5 mM 4-methylpyrazole (4-MP), an inhibitor of ethanol metabolism. Slices from every time point (24, 48, 72, and 96 h) were examined for glutathione (GSH) levels, lipid peroxidation [thiobarbituric acid-reactive substance (TBARS) assay], cytokine production (ELISA and RT-PCR), and myofibroblast activation [immunoblotting and immunohistochemistry for smooth muscle actin (SMA) and collagen]. Treatment of PCLS with 25 mM ethanol induced significant oxidative stress within 24 h, including depletion of cellular GSH and increased lipid peroxidation compared with controls ( P < 0.05). Ethanol treatment also elicited a significant and sustained increase in interleukin-6 (IL-6) production ( P < 0.05). Importantly, ethanol treatment accelerates a fibrogenic response after 48 h, represented by significant increases in SMA and collagen 1α(I) production ( P < 0.05). These ethanol-induced effects were prevented by the addition of 4-MP. Ethanol metabolism induces oxidative stress (GSH depletion and increased lipid peroxidation) and sustained IL-6 expression in rat PCLS. These phenomena precede and coincide with myofibroblast activation, which occurs within 48 h of treatment. These results indicate the PCLS can be used as in vitro model for studying multicellular interactions during the early stages of ethanol-induced liver injury and fibrogenesis.


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