Zn 2+ induced molecular responses associated with oxidative stress, DNA damage and histopathological lesions in liver and kidney of the fish, Channa punctatus (Bloch, 1793)

2018 ◽  
Vol 151 ◽  
pp. 10-20 ◽  
Author(s):  
Arun Ratn ◽  
Rajesh Prasad ◽  
Yashika Awasthi ◽  
Manoj Kumar ◽  
Abha Misra ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Channa Punctatus ◽  
Molecular Responses ◽  
Histopathological Lesions ◽  
Liver And Kidney

Phorate induced oxidative stress, DNA damage and differential expression of p53, apaf-1 and cat genes in fish, Channa punctatus (Bloch, 1793)

Chemosphere ◽  
2017 ◽  
Vol 182 ◽  
pp. 382-391 ◽  
Author(s):  
Arun Ratn ◽  
Yashika Awasthi ◽  
Manoj Kumar ◽  
Sunil Kumar Singh ◽  
Renu Tripathi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Differential Expression ◽  
Channa Punctatus

scholarly journals Oxidative Stress and DNA Damage Induced by Chromium in Liver and Kidney of Goldfish, Carassius auratus

2013 ◽  
Vol 8 ◽  
pp. BMI.S11456 ◽  
Author(s):  
Venkatramreddy Velma ◽  
Paul B. Tchounwou
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Carassius Auratus ◽  
Industrial Effluents ◽  
Lipid Hydroperoxides ◽  
Kidney Cells ◽  
Surrounding Water ◽  
Goldfish Carassius Auratus ◽  
Liver And Kidney ◽  
Abundant Element

Chromium (Cr) is an abundant element in the Earth's crust. It exhibits various oxidation states, from divalent to hexavalent forms. Cr has diverse applications in various industrial processes and inadequate treatment of the industrial effluents leads to the contamination of the surrounding water resources. Hexavalent chromium (Cr (VI)) is the most toxic form, and its toxicity has been associated with oxidative stress. The present study was designed to investigate the toxic potential of Cr (VI) in fish. In this research, we investigated the role of oxidative stress in chromium-induced genotoxicity in the liver and kidney cells of goldfish, Carassius auratus. Goldfish were acclimatized to the laboratory conditions and exposed them to 5% and 10% of 96 hr-LC50 (85.7 mg/L) of aqueous Cr (VI) in a continuous flow through system. Fish were sampled every 7 days for a period of 28 days to analyze the lipid hydroperoxides (LHP) levels and genotoxic potentials in the liver and kidney. LHP levels were analyzed by spectrophotometry while genotoxicity was assessed by single cell gel electrophoresis (comet) assay. LHP levels in the liver increased significantly at week 1, followed by a decrease. LHP levels in the kidney increased significantly at weeks 1, 2, and 3, and decreased at week 4 compared to the control. The percentage of DNA damage increased in both liver and kidney at both test concentrations. The results clearly indicate that Cr (VI) induces significant levels of DNA damage in liver and kidney cells of goldfish. The induced LHP levels in both organs were concentration-dependent and were directly correlated with the levels of DNA damage. The two tested Cr (VI) concentrations induced significant levels of oxidative stress in both organs, however the kidney appears to be more vulnerable and sensitive to Cr-induced toxicity than the liver.

scholarly journals The Protective Effect of Naringenin-Oxime on Cisplatin-Induced Toxicity in Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Ismail Koyuncu ◽  
Abdurrahim Kocyigit ◽  
Ataman Gonel ◽  
Erkan Arslan ◽  
Mustafa Durgun
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Comet Assay ◽  
Protective Effect ◽  
Stress Index ◽  
Mononuclear Leukocytes ◽  
Albino Rats ◽  
Peripheral Blood Mononuclear ◽  
Liver And Kidney ◽  
And Oxidative Stress

The aim of this study is to examine the protective effect of naringenin-oxime (NOX) on cisplatin-induced major organ toxicity and DNA damage in rats. Thirty-five male Wistar albino rats were equally split into five groups as follows: control (i.p., 0.1 ml of saline), Cis administration (i.p., 7 mg/kg b.w.), NOX treatment (i.p., 20 mg/kg b.w., daily for ten days), Cis + NOX20, and Cis + NOX40 combination (i.p., 20 and 40 mg/kg b.w., daily for ten days). Serum and peripheral blood mononuclear leukocytes (PBMC) were obtained from blood. Malondialdehyde, glutathione, total antioxidant and oxidant status, and catalase were measured in serum, liver, and kidney, and oxidative stress index was calculated. In parallel, paraoxonase and arylesterase activities were tested in liver and serum. We used 8-OHdOG as a marker for DNA damage in serum via ELISA and in PMBC via comet assay. Treatment with Cis elevated the levels of serum biochemical parameters, oxidative stress, and DNA damage. Pretreatments of NOX restored biochemical and oxidative stress parameters in serum, renal, and liver tissues (p<0.01) and reduced 8-OHdG level, a finding further supported by comet assay in PBMC. Observations of the present study support the fact that treatment with NOX prevents Cis-induced hepatotoxicity, nephrotoxicity, and genotoxicity by restoring antioxidant system.

scholarly journals Cerium Oxide Nanoparticles in Lung Acutely Induce Oxidative Stress, Inflammation, and DNA Damage in Various Organs of Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Abderrahim Nemmar ◽  
Priya Yuvaraju ◽  
Sumaya Beegam ◽  
Mohamed A. Fahim ◽  
Badreldin H. Ali
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Health Concern ◽  
Fuel Additive ◽  
Limited Information ◽  
Pulmonary Exposure ◽  
Multiple Organs ◽  
Liver And Kidney ◽  
Necrosis Factor

CeO2 nanoparticles (CeO2 NPs) which are used as a diesel fuel additive are emitted in the particulate phase in the exhaust, posing a health concern. However, limited information exists regarding the in vivo acute toxicity of CeO2 NPs on multiple organs. Presently, we investigated the acute (24 h) effects of intratracheally instilled CeO2 NPs in mice (0.5 mg/kg) on oxidative stress, inflammation, and DNA damage in major organs including lung, heart, liver, kidneys, spleen, and brain. Lipid peroxidation measured by malondialdehyde production was increased in the lungs only, and reactive oxygen species were increased in the lung, heart, kidney, and brain. Superoxide dismutase activity was decreased in the lung, liver, and kidney, whereas glutathione increased in lung but it decreased in the kidney. Total nitric oxide was increased in the lung and spleen but it decreased in the heart. Tumour necrosis factor-α increased in all organs studied. Interleukin- (IL-) 6 increased in the lung, heart, liver, kidney, and spleen. IL-1β augmented in the lung, heart, kidney, and spleen. Moreover, CeO2 NPs induced DNA damage, assessed by COMET assay, in all organs studied. Collectively, these findings indicate that pulmonary exposure to CeO2 NPs causes oxidative stress, inflammation, and DNA damage in multiple organs.

DNA damage and oxidative stress modulatory effects of glyphosate-based herbicide in freshwater fish, Channa punctatus

2013 ◽  
Vol 36 (2) ◽  
pp. 539-547 ◽  
Author(s):  
C.D. Nwani ◽  
N.S. Nagpure ◽  
Ravindra Kumar ◽  
Basdeo Kushwaha ◽  
W.S. Lakra
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Freshwater Fish ◽  
Channa Punctatus ◽  
And Oxidative Stress

scholarly journals Effects of primaquine and chloroquine on oxidative stress parameters in rats

2015 ◽  
Vol 87 (2 suppl) ◽  
pp. 1487-1496 ◽  
Author(s):  
FRANCIANNE GIOVANELLA ◽  
GABRIELA K. FERREIRA ◽  
SAMIRA D.T. DE PRÁ ◽  
MILENA CARVALHO-SILVA ◽  
LARA M. GOMES ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Oxidative Damage ◽  
Protein Carbonyls ◽  
Prolonged Treatment ◽  
Oxidative Stress Parameters ◽  
Chloroquine Treatment ◽  
Liver And Kidney ◽  
The Brain ◽  
Stress Parameters

Primaquine and chloroquine are used for the treatment of malaria; evidence from the literature suggests that these drugs may induce oxidative stress. In this study we investigated the effects of primaquine and chloroquine on oxidative damage and DNA damage in brain, liver and kidney of rats after 7, 14 and 21 days of administration. Our results demonstrated that primaquine causes DNA damage in brain after 7, 14 and 21 days, and in liver after 7 and 14 days. Moreover, primaquine increases TBARS levels in the kidney and protein carbonyls in the brain after 14 days, and decreases protein carbonyls in the liver after 7 days. Whereas chloroquine causes DNA damage in the kidney after 7 and 14 days, and in the liver after 14 and 21 days, increases TBARS levels in the kidney after 7 days, and decreases TBARS levels in the brain after 21 days. Moreover, decreases protein carbonyls in the liver after 7 and 14 days, and in the brain after 7 and 21 days. However, chloroquine treatment for 14 days increases protein carbonyls in the brain and kidney. In conclusion, these results showed that prolonged treatment with antimalarial may adversely affect the DNA.

scholarly journals Heteroxenia Ghardaqensis Extract Protects Against DNA Damage in Streptozotocin-Induced Experimental Diabetes

2019 ◽  
Vol 12 (1) ◽  
pp. 71-78 ◽  
Author(s):  
Abdel Razik Farrag ◽  
Mahmoud Nassar ◽  
Zakaria El-Khayat ◽  
Jihan Hussein ◽  
Nadia Ahmed Mohammed ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Dna Damage ◽  
Body Weight ◽  
Experimental Period ◽  
Reversed Phase ◽  
Diabetic Rats ◽  
Albino Rats ◽  
Liver And Kidney

DNA damage is correlated to type-2 diabetes mellitus (T2DM) and its complications via oxidative stress. This study aimed to evaluate the anti-diabetic effect of Heteroxenia ghardaqensis extract on streptozotocin (STZ) induced-diabetes and how far can this extract attenuate DNA damage in this model. Forty male albino rats (160-180 g) were used in this study and divided into four groups: control, diabetic, diabetic rats received H. ghardaqensis extract (30 mg/kg body weight/day) orally for four weeks and diabetic rats received H. ghardaqensis extract (60 mg/kg body weight/day) orally for four weeks. After the experimental period, fasting blood sugar and serum cholesterol were determined. Urinary 8-hydroxyguanosine (8-OHdG) as a marker of DNA damage was estimated by reversed phase (HPLC). Liver and kidney nitic oxide (NO) and malondialdehyde (MDA) were estimated. Pancreatic tissues were histopathologicaly examined. Our results suggested that diabetes mellitus is accompanied by elevation of DNA damage that enhances the tendency to mutagens and reduce the efficacy of DNA repair. H. ghardaqensis extract appeared to be effective against the oxidative stress induced by STZ which may be due to sesquiterpenoids and diterpenes compounds that scavenge free radicals and increase the antioxidant enzymes as appeared in attenuation of DNA damage.

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