Cadmium acts as a silent killer of liver by inducing oxidative stress and hepatocellular injury and a possible amelioration by vitamin B12 and folic acid in rat model

2019 ◽  
Vol 1 ◽  
pp. 105-117
Author(s):  
A. Banerjee ◽  
P. Nandi ◽  
C. Bhattacharya ◽  
Z. Kabir ◽  
S. Mukherjee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Folic Acid ◽  
Vitamin B12 ◽  
Rat Model ◽  
Male Rats ◽  
Albino Rats ◽  
Therapeutic Effects ◽  
Hepatocellular Injury ◽  
Male Adult ◽  
Wistar Albino Rats

<br/><b>Purpose:</b> To investigate the involvement of oxidative stress in Cadmium (Cd) induced alteration in the functional status of the liver. And to assess the efficacy of folic acid and vitamin B12 in preventing Cd-induced damage in the same. <br/><b>Materials and methods:</b> The experiment was carried out for four weeks. For the experiment, 25 healthy male adult Wistar albino rats were randomly selected and were divided into five equal groups and treated as control, treated with Cd, supplemented with vitamin B12 and folic acid and in the combination of these two. After 28 days the liver function enzymes and oxidative stress parameters were measured. <br/><b>Results:</b> Cd is the silent killer of the hepatic system through the induction of oxidative stress in male rats. From this investigation, it is evident that the folic acid+vitamin B12 possess significant hepatoprotective and antioxidant activity against Cd-induced hepatotoxicity in the rat model. In addition, results revealed that the folic acid alone and or in combination with vitamin B12 blunted the hepatotoxic effect significantly. <br/><b>Conclusions:</b> Based on results obtained, it can be concluded that folic acid and vitamin B12 offer a protective effect in Cd-induced oxidative stress associated with hepatocellular injury. Folic acid and vitamin B12 can be considered as a potent natural antioxidant which has the capacity to provide protection against Cd-induced oxidative stress in the liver in rats. However, to elucidate the exact mechanism of this modulatory effect and to examine its potential therapeutic effects further studies are essential.

Beneficial effects of quercetin on renal injury and oxidative stress caused by ciprofloxacin in rats

2015 ◽  
Vol 35 (3) ◽  
pp. 276-281 ◽  
Author(s):  
H Elbe ◽  
Z Dogan ◽  
E Taslidere ◽  
A Cetin ◽  
Y Turkoz
Keyword(s):  
Oxidative Stress ◽  
Renal Injury ◽  
Kidney Tissue ◽  
Albino Rats ◽  
Therapeutic Effects ◽  
Histopathological Changes ◽  
Tubular Atrophy ◽  
Beneficial Effects ◽  
Wistar Albino Rats ◽  
And Oxidative Stress

Ciprofloxacin is a broad-spectrum quinolone antibiotic commonly used in clinical practice. Quercetin is an antioxidant belongs to flavonoid group. It inhibits the production of superoxide anion. In this study, we aimed to evaluate the effects of quercetin on renal injury and oxidative stress caused by ciprofloxacin. Twenty-eight female Wistar albino rats were divided into four groups: control, quercetin (20 mg kg−1 day−1 gavage for 21 days), ciprofloxacin (20 mg kg−1 twice a day intraperitoneally for 10 days), and ciprofloxacin + quercetin. Samples were processed for histological and biochemical evaluations. Malondialdehyde (MDA) and glutathione (GSH) levels, superoxide dismutase (SOD), and catalase (CAT) activities were measured in kidney tissue. The ciprofloxacin group showed histopathological changes such as infiltration, dilatation in tubules, tubular atrophy, reduction of Bowman’s space, congestion, hemorrhage, and necrosis. In the ciprofloxacin + quercetin group, these histopathological changes markedly reduced. MDA levels increased in the ciprofloxacin group and decreased in the ciptofloxacin + quercetin group. SOD and CAT activities and GSH levels significantly decreased in the ciprofloxacin group. On the other hand, in the ciprofloxacin + quercetin group, SOD and CAT activities and GSH levels significantly increased with regard to the ciprofloxacin group. We concluded that quercetin has antioxidative and therapeutic effects on renal injury and oxidative stress caused by ciprofloxacin in rats.

scholarly journals The influence of subchronic co-application of vitamins B6 and folic acid on cardiac oxidative stress and biochemical markers in monocrotaline-induced heart failure in male Wistar albino rats

2020 ◽  
Vol 98 (2) ◽  
pp. 93-102 ◽  
Author(s):  
Jovana Jakovljevic Uzelac ◽  
Tatjana Djukic ◽  
Slavica Mutavdzin ◽  
Sanja Stankovic ◽  
Milica Labudovic Borovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Folic Acid ◽  
Vitamin B6 ◽  
Cardiac Tissue ◽  
Troponin T ◽  
Physiological Saline ◽  
Albino Rats ◽  
Wistar Albino Rats ◽  
The Right

The aim of this study was to test the hypothesis that subchronic co-application of vitamins B6 and folic acid (FA) could affect heart failure (HF) induced by monocrotaline (MCT), with the modulation of oxidative stress parameters and cardiometabolic biomarkers. Biochemical and histomorphometric analyses were assessed in blank solution-exposed controls (C1 physiological saline 1 mL/kg, 1 day, n = 8; C2 physiological saline 1 mL/kg, 28 days, n = 8), MCT-induced HF (MCT 50 mg/kg, n = 8), B6+FA (vitamin B6 7 mg·kg–1·day–1, FA 5 mg·kg–1·day–1; n = 8), and MCT+B6+FA (MCT 50 mg/kg, vitamin B6 7 mg·kg–1·day–1, FA 5 mg·kg–1·day–1; n = 8) in male Wistar albino rats (body mass 160 g at the start). Superoxide dismutase and glutathione peroxidase activities, thiol-, carbonyl groups, and nitrotyrosine were determined in cardiac tissue. Echocardiography was performed to confirm MCT-induced HF. The right ventricular wall hypertrophy, accompanied with significant increase of troponin T and preserved renal and liver function, has been shown in MCT-induced HF. However, these effects were not related to antioxidant effects of vitamin B6 and FA, since several parameters of oxidative stress were more pronounced after treatment. In this study, co-application of vitamins B6 and FA did not attenuate hypertrophy of the right ventricle wall but aggravated oxidative stress, which is involved in HF pathogenesis.

scholarly journals Role of Oats in Ameliorating Hepatic and Renal Toxicity Induced by Acute Lead Nanoparticles in Male Rats

2020 ◽  
pp. 38-45
Author(s):  
Sarah Alashmouni ◽  
Afaf El- Atrash ◽  
Manar Kandeel ◽  
Ehab Tousson
Keyword(s):  
Renal Damage ◽  
Chloride Ions ◽  
The Body ◽  
Male Rats ◽  
Control Group ◽  
Albino Rats ◽  
Sufficient Information ◽  
Therapeutic Effects ◽  
Male Adult ◽  
Organ Systems

Aims: Lead is well known environmental pollutant, which can cause toxic effects in multiple organ systems. Lead originates from various industrial and/or household sources, and enters the body through food and fluid intakes, as well as by inhalation. No sufficient information present about the toxic effect of acute lead nanoparticles on kidney and liver. Accordingly, current study was performed to study the therapeutic effects of Oats extract towards the injection of lead nanoparticles (Pb NPs) in rat induced kidney and liver damage by increasing kidney and liver functions, and electrolytes. Study Design:  A total of 40 male adult albino rats were equally divided into four groups (Control group, Oats group, Pb NPs group as acute toxicity and last group is Pb NPs +Oats). Results: Current results revealed that; a significant increase in the levels of serum aspartate transaminase (AST) and alanine transaminase (ALT), alkaline phosphatase (ALP), urea, creatinine, potassium and chloride ions after injection with Pb NPs as compared to control group. In contrast; a significant decrease in serum albumin, total proteins, and sodium ions in Pb NPs as compared to control groups. Treatment of Pb NPs with Oats improved this change in liver and kidney functions as compared to Pb NPs group. Conclusion: These findings suggested that; lead nanoparticles injection induced hepatic and renal damage. This shows that the desired dose of Pb NPs can safely be used with Oats in improving hepatic and renal damage in toxic group in young rats.

scholarly journals Effects of cisplatin on lipid peroxidation and the glutathione redox status in the liver of male rats: The protective role of selenium

2010 ◽  
Vol 62 (1) ◽  
pp. 75-82 ◽  
Author(s):  
Ivana Trbojevic ◽  
Branka Ognjanovic ◽  
Natasa Djordjevic ◽  
Snezana Markovic ◽  
A.S. Stajn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Membrane Lipids ◽  
Redox Status ◽  
Protective Role ◽  
Male Rats ◽  
Albino Rats ◽  
Wistar Albino Rats ◽  
Glutathione Redox

The role of oxidative stress in cisplatin (CP) toxicity and its prevention by pretreatment with selenium (Se) was investigated. Male Wistar albino rats were injected with a single dose of cisplatin (7.5 mg CP/kg b.m., i.p.) and selenium (6 mg Se/kg b.m, as Na2SeO3, i.p.) alone or in combination. The results suggest that CP intoxication induces oxidative stress and alters the glutathione redox status: reduced glutathione (GSH), oxidized glutathione (GSSG) and the GSH/GSSG ratio (GSH RI), resulting in increased lipid peroxidation (LPO) in rat liver. The pretreatment with selenium prior to CP treatment showed a protective effect against the toxic influence of CP on peroxidation of the membrane lipids and an altering of the glutathione redox status in the liver of rats. From our results we conclude that selenium functions as a potent antioxidant and suggest that it can control CP-induced hepatotoxicity in rats.

scholarly journals Folic acid and vitamin B12 ameliorate nicotine-induced testicular toxicity in rats

Biomedicine ◽  
2020 ◽  
Vol 39 (2) ◽  
pp. 353-368
Author(s):  
Dibyendu Ray ◽  
Ankita Bhattacharjee ◽  
Oly Banerjee ◽  
Shilpi Kumari Prasad ◽  
Siddhartha Singh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Folic Acid ◽  
Cigarette Smoking ◽  
Vitamin B12 ◽  
Inflammatory Cytokines ◽  
Reproductive Toxicity ◽  
Testicular Tissue ◽  
Albino Rats ◽  
Pro Inflammatory Cytokines

Introduction and Aim: Cigarette smoking, one of the fundamental roots of preventable morbidity, has a myriad of notorious effects. Nicotine is the most bountiful and symbolic constituent of cigarette smoke. The liaison between smoking and infertility has been investigated for decades; but it’s still dubious whether the noxious effects of cigarette smoking on testis and sperm characteristics are by virtue of nicotine. Therefore, the current study interrogated the ameliorative effects of folic acid and vitamin B12 on nicotine induced catastrophe in testicular tissue and sperm characters in male albino rats. Materials and Methods: Rats were treated with nicotine (3 mg/kg body weight/day, intraperitoneal) with or without folic acid (36µg/kg body weight/day, orally) and vitamin B12 (0.63µg/kg body weight/ day, orally) for 21 days. Sperm qualities were analyzed for motility and morphology. Various oxidative and anti- oxidative stress parameters, pro inflammatory cytokines levels, hormonal assays were performed. Results: Findings marked that nicotine caused degenerative changes in the testicular tissue. Supplementation with folic acid and vitamin B12 reversed these results along with suppressing the nicotine induced changes in TNF- ?, IL-6, and markers of oxidative stress. Moreover, folic acid and vitamin B12 in combination also significantly blunted the altered activities of testicular key androgenic enzymes, plasma levels of testosterone, LH, and FSH following nicotine exposure. Conclusion: In closure, testimonies manifested that folic acid and vitamin B12 may act as plausible strategy against oxidative stress, which is a pivotal step in nicotine-induced reproductive toxicity, and bettering functional status of testicular tissue by scavenging free radicals and hindering the generation of pro- inflammatory cytokines.  

Fetuin-A exerts a protective effect against experimentally induced intestinal ischemia/reperfusion by suppressing autophagic cell death

2021 ◽  
pp. 153537022199520
Author(s):  
Nanees F El-Malkey ◽  
Amira E Alsemeh ◽  
Wesam MR Ashour ◽  
Nancy H Hassan ◽  
Husam M Edrees
Keyword(s):  
Oxidative Stress ◽  
Rat Model ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Protective Role ◽  
Beclin 1 ◽  
Male Rats ◽  
Fetuin A ◽  
Intestinal Ischemia Reperfusion ◽  
And Oxidative Stress

Intestinal tissue is highly susceptible to ischemia/reperfusion injury in many hazardous health conditions. The anti-inflammatory and antioxidant glycoprotein fetuin-A showed efficacy in cerebral ischemic injury; however, its protective role against intestinal ischemia/reperfusion remains elusive. Therefore, this study investigated the protective role of fetuin-A supplementation against intestinal structural changes and dysfunction in a rat model of intestinal ischemia/reperfusion. We equally divided 72 male rats into control, sham, ischemia/reperfusion, and fetuin-A-pretreated ischemia/reperfusion (100 mg/kg/day fetuin-A intraperitoneally for three days prior to surgery and a third dose 1 h prior to the experiment) groups. After 2 h of reperfusion, the jejunum was dissected and examined for spontaneous contractility. A jejunal homogenate was used to assess inflammatory and oxidative stress enzymes. Staining of histological sections was carried out with hematoxylin, eosin and Masson’s trichrome stain for evaluation. Immunohistochemistry was performed to detect autophagy proteins beclin-1, LC3, and p62. This study found that fetuin-A significantly improved ischemia/reperfusion-induced mucosal injury by reducing the percentage of areas of collagen deposition, increasing the amplitude of spontaneous contraction, decreasing inflammation and oxidative stress, and upregulating p62 expression, which was accompanied by beclin-1 and LC3 downregulation. Our findings suggest that fetuin-A treatment can prevent ischemia/reperfusion-induced jejunal structural and functional changes by increasing antioxidant activity and regulating autophagy disturbances observed in the ischemia/reperfusion rat model. Furthermore, fetuin-A may provide a protective influence against intestinal ischemia/reperfusion complications.

Effects of erdosteine on cyclosporin-A-induced nephrotoxicity

2011 ◽  
Vol 31 (6) ◽  
pp. 565-573 ◽  
Author(s):  
M Tutanc ◽  
V Arica ◽  
N Yılmaz ◽  
A Nacar ◽  
I Zararsiz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cyclosporin A ◽  
Protective Role ◽  
Control Group ◽  
Albino Rats ◽  
Protective Mechanism ◽  
Antioxidant Parameters ◽  
Group 2 ◽  
Wistar Albino Rats

Aim: In cyclosporin-A (CsA)-induced toxicity, oxidative stress has been implicated as a potential responsible mechanism. Therefore, we aimed to investigate the protective role of erdosteine against CsA-induced nephrotoxicity in terms of tissue oxidant/antioxidant parameters and light microscopy in rats. Materials and methods: Wistar albino rats were randomly separated into four groups. Group 1 rats treated with sodium chloride served as the control, group 2 rats were treated with CsA, group 3 with CsA plus erdosteine, and group 4 with erdosteine alone. Animals were killed and blood samples were analyzed for blood urea nitrogen (BUN), serum creatinine (Cr), uric acid (UA), total protein (TP), and albumin (ALB) levels. Kidney sections were analyzed for malondialdehyde (MDA) and nitric oxide (NO) levels and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as for histopathological changes. Results: In the CsA group, MDA, GSH-Px, BUN, and Cr levels were increased. The TP and ALB levels were decreased. These changes had been improved by erdosteine administration. Other biochemical parameters did not show any significant change. Conclusion: These results indicate that erdosteine produces a protective mechanism against CsA-induced nephrotoxicity and suggest a role of oxidative stress in pathogenesis.

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