The Effect of Thymol on Renal Toxicity Induced by Mercury Chloride in Rats

2021 ◽  
Author(s):  
Hamid Reza Jamshidi ◽  
Faezeh Taheri
Keyword(s):  
Mercuric Chloride ◽  
Renal Toxicity ◽  
Corn Oil ◽  
Kidney Tissue ◽  
Control Group ◽  
Mercury Chloride ◽  
Protective Effects ◽  
Tissue Samples ◽  
Significant Difference ◽  
Anti Oxidant

Background and Aims: Mercuric chloride is highly toxic once absorbed into the bloodstream, especially the kidneys in which it is collected. Mercury chloride increases hydrogen peroxide and enhances the destruction of protective enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPX), leading to oxidative stress. Besides, thymol has anti-oxidant effects and can increase the activity of SOD and GPX. This study aims to evaluate the efficacy of thymol on mercury chloride-induced toxicity. Materials and Methods: In this study, 30 rats, consisting of 6 groups of 5, were used. Control group receiving a single dose of 0.5 mg/kg mercuric chloride for 15 days, third, fourth, and fifth group received intraperitoneal injection of mercuric chloride at a dose of 0.5 mg/kg for 15 days plus thymol at a dose of 10, 30, 50 mg/kg. The sixth group received mercuric chloride at a dose of 0.5 mg/kg for 15 days plus thymol at 30 mg/kg per day for ten days. Results: Results showed a significant difference in the activity of catalase enzyme in kidney tissue samples test. According to the results of SOD, there is a significant difference between the group of corn oil and the group of mercury chloride and between the group of mercury chloride and the group that receives thymol at a dose of 10, 30, 50 mg/kg (p ≤ 0.05). Conclusions: It can be concluded that mercury chloride-induced kidney toxicity and thymol have anti-oxidant protective effects for SOD and GPX.

Effect of Sodium Selenide on Renal Toxicity Induced By Mercuric Chloride in Rat

2020 ◽  
Author(s):  
Hamid Reza Jamshidi ◽  
Hasti Kalantar
Keyword(s):  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Data Analysis ◽  
Vitamin E ◽  
Protective Effect ◽  
Mercuric Chloride ◽  
Renal Toxicity ◽  
Kidney Tissue ◽  
Control Group ◽  
Significant Difference

Background and Aims: Mercury, with its oxidative activity, causes damage to the antioxidant enzymes thus resulting in physiological disorders. Sodium selenide is an antioxidant that protects antioxidant enzymes. The aim of this study was to investigate the protective effect of sodium selenide on renal toxicity induced by mercuric chloride in rats. Materials and Methods: Animals were divided into 6 groups of 6 each. Control group was treated with mercuric chloride (2.5 mg/kg) subcutaneously. Groups 2, 3 and 4 of the rats were treated with 2.5 mg/kg of mercuric chloride and sodium selenide subcutaneously administered at doses of 0.02, 0.04 and 0.08 mg/kg, respectively. The fifth group received 0.04 mg/kg sodium selenide subcutaneously after 25 days of mercuric chloride (2.5 mg/kg) treatment. The sixth group was treated with 2.5 mg/kg of mercuric chloride subcutaneously and 100 mg/kg of vitamin E by gavage. Results: After data analysis of the activity of the enzyme catalase, superoxide dismutase, glutathione peroxide, creatinine and urea, there was a significant difference in the activity of these factors compared with the control group in blood and kidney tissue (p<0.05). Conclusions: This study indicated that mercuric chloride has toxic effects in blood and kidney and sodium selenide may be able to reduce its’ blood and renal toxicity.

scholarly journals Histological and Hormonal Study of the Protective Effect of the Calotropis Procera Against the Toxicity of Mercury Chloride

2020 ◽  
pp. 5-14
Author(s):  
Leila Belfarhi ◽  
Ibtissem Chouba ◽  
Naziha Amri ◽  
Nadia Boukris ◽  
Abdelkrim Tahraoui
Keyword(s):  
Mercuric Chloride ◽  
Female Rats ◽  
Male Rats ◽  
Calotropis Procera ◽  
Control Group ◽  
Mercury Chloride ◽  
Protective Effects ◽  
Male And Female ◽  
Male And Female Rats ◽  
Group I

We undertook this study with the aim of investigating the detoxification of an extreme toxic metal mercury chloride by the Calotropis procera plant taken from the Algerian Sahara. We studied the protective effects of the plant Calotropis procera against renal toxicity and Mercury chloride-induced hepatic. Ten male and female albino rats Wistar were divided into four equal groups. Group (I) served as a healthy control group, group (II) were intra-peritoneal administered with 10 ml of Calotropis procera, group (III) were intra-peritoneal administrated with both 10 ml of the plant Calotropis procera and 0.2 mg of mercuric chloride (HgCl2) and group (IV) were intraperitoneal administrated with both 0.2 mg of mercuric chlorid (HgCl2) and 10 ml of the plant Calotropis. All groups were treated for 20 days. Mercury chloride causes a slight increase in glomerular cellularitis in the kidneys of male and female rats. Treatment with Calotropis procera had significantly improving protective effects of kidney of female rats from toxicity of mercuric chloride. Calotropis procera causes a thyroid-like appearance in the glomeruli of the male kidneys to hide the lesions of mercury chloride. Our results have shown that the plant Calotropis procera completely protects the liver of female rats against the toxicity of mercury chloride. In the liver of male rats, mercury chloride causes macro-vacuolar steatosis. Treatment with Calotrpois procera hid the hepatic steatosis of male rats and centralized them in the center under the aspect of peri-centro-lobular medio-vacuolar steatosis. Mercuric chloride caused a decrease in the secretion of the hormone ACTH in the group of male and female rats. Treatment with Calotropis procera caused increased ACTH levels in female rats and did not cause ACTH changes in male rats. Our results demonstrate from hormone analyzes of the hormone ACTH that female rats are resistant more than male rats via the toxicity of mercury chloride.

scholarly journals Impact of Pycnogenol on Acetaminophen-Induced Hepatorenal Damage

2021 ◽  
Vol 12 (6) ◽  
pp. 8070-8080
Keyword(s):  
Inflammatory Cytokines ◽  
Kidney Tissue ◽  
Albino Rats ◽  
Myeloperoxidase Activity ◽  
Protective Effects ◽  
Tissue Samples ◽  
Liver And Kidney ◽  
Anti Oxidant ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

We investigated the protective effects of pycnogenol (PYC), a natural anti-oxidant with an anti-inflammatory effect, on the acetaminophen (APAP)-induced hepatorenal injury in rats. Wistar albino rats were divided into four experimental groups: control, PYC (10 mg/kg, ip), APAP (1000 mg/kg), and APAP+PYC groups. Rats were decapitated 24 hours after the APAP injection, and their blood was taken to determine blood urea nitrogen (BUN), creatinine, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and pro-inflammatory cytokines; TNF-α and IL-1 β. Liver and kidney tissue samples were obtained for the histological examination and the determination of malondialdehyde (MDA) and glutathione (GSH) levels as well as myeloperoxidase (MPO) and Na+/K+-ATPase activities. PYC treatment decreased the APAP-induced elevations in serum pro-inflammatory cytokines and reduced the impairment of liver and kidney functions. Furthermore, the increase in tissue lipid peroxidation and myeloperoxidase activity and the decrease in the GSH levels and Na+/K+-ATPase activity by the APAP overdose were reversed by the PYC treatment. Besides, histologic findings reinforce the protective effect of PYC in APAP-induced hepatorenal damage. PYC, which appears to have restored the GSH and depressed neutrophil infiltration and the associated release of pro-inflammatory cytokines, merits consideration as an anti-oxidant and anti-inflammatory agent in preventing APAP-induced hepatorenal damage.

Effect of Vitamin E as α-Tocopherol Acetate on Mercuric Chloride-Induced Chronic Oxidoreductive Stress and Nephrotoxicity in Rats

2019 ◽  
Vol 43 (2) ◽  
pp. 98-108
Author(s):  
Ajwad Awad Muhammad Assumaidaee
Keyword(s):  
Vitamin E ◽  
Mercuric Chloride ◽  
Renal Toxicity ◽  
Lethal Dose ◽  
Control Group ◽  
Albino Rats ◽  
Protective Effects ◽  
Beneficial Effects ◽  
Tocopherol Acetate ◽  
Serum Biochemical

Impact of vitamin E against mercuric chloride (HgCL2) induced renal toxicity in Wister albino rats was studied. Feeding of the rats with diet and water contaminated with a non lethal dose of the mercuric chloride (20 parts per million) every other day for 42 days resulted in significant increase of serum malondialdehyde (MDA), which is an important biomarker of the oxidoreductive stress, and significant decline in each of the reduced glutathione (r-GSH) concentration, glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) enzymes activities, which constitute a vital part of the endogenous protective antioxidant system, as compared to the control group. The study found that the simultaneous oral co administration of vitamin E (as α-tocopherol acetate) 100 mg/kg B.W. every other day for 42 days along with mercuric chloride produced a cardinal protective effects against the development of the mercuric chloride induced nephrotoxicity. This can be through reversing the elevated oxidative stress; induced by the administration of the HgCL2. In conclusion serum biochemical and kidney histopathological findings of the current study highlight the beneficial effects of vitamin E in rats with HgCl2-mediated renal toxicity.

scholarly journals Nephroprotective effects of eriocitrin via alleviation of oxidative stress and DNA damage against cisplatin-induced renal toxicity

2020 ◽  
Vol 45 (4) ◽  
pp. 381-388
Author(s):  
Yongsheng Jing ◽  
Xiaoqing Wu ◽  
Huili Jiang ◽  
Rong Wang
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Normal Control ◽  
Renal Toxicity ◽  
Kidney Tissue ◽  
Protective Measure ◽  
Control Group ◽  
Tissue Samples ◽  
Tnf Α ◽  
Cytokine Levels

AbstractBackgroundCisplatin, a common anti-neoplastic drug used in the medical industry for cancer treatment has shown adverse nephrotoxic effects. This research targets to demonstrate the protective measure of eriocitrin, a bioactive flavonoid, against cisplatin-induced renal toxicity in rats.Materials and methodsRats of normal control and model groups were treated with saline whereas experimental groups received oral administration of eriocitrin (25 and 50 mg/kg b.w.) for 10 days and a single intraperitoneal (i.p.) injection of cisplatin (8 mg/kg b.w.) was given on the 7th day for all except normal control group. Blood serum, urine, and kidney tissue samples were collected for analysis.ResultsCisplatin-induced rats demonstrated significant renal toxicity and damage. Eriocitrin dose-dependently reversed the effects by decreasing the proteinuria in urine, and urea, creatinine, lipid peroxidation, nitric oxide (NO) and pro-inflammatory cytokine levels (TNF-α, IL-1β) in serum. The tissue levels of reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) were increased, whereas the levels of tissue DNA fragmentation and serum PARP-1 and Caspase-3 were reduced against model group. Histopathological modulations were supporting the protective effect of eriocitrin.ConclusionEriocitrin has significant nephroprotective effects against cisplatin-induced renal toxicity by alleviating oxidative stress, preventing apoptosis and DNA damage.

scholarly journals The Effect of Zingiber officinale on the Spleen Tissue and Antibody Titer of Broiler Chickens

2019 ◽  
Vol 36 (01) ◽  
pp. 046-050
Author(s):  
Alireza Taghdisi ◽  
Sajjad Hejazi
Keyword(s):  
Broiler Chickens ◽  
Zingiber Officinale ◽  
Control Group ◽  
White Pulp ◽  
Broiler Chicks ◽  
Pulp Tissue ◽  
Tissue Samples ◽  
Serum Factors ◽  
Spleen Tissue ◽  
Significant Difference

Introduction Increasing the immune system's function of fighting infectious diseases is very important in the poultry industry. Ginger, scientifically known as Zingiber officinale, belongs to the Zingiberaceae family. The use of ginger in the diet of poultry increases serum levels of superoxide dismutase enzymes and glutathione peroxidase, which are considered to be important antioxidant enzymes. The main objective of the present study is to evaluate the effect of ginger on the spleen tissue of broiler chickens. Material and Methods The specimens comprised 2 groups of 20 Ross breed broiler chicks, for 42 days and were then, examined and tested. The diet was supplemented with 1 g/kg of ginger powder from the beginning of the rearing period. Blood samples of the chicks were randomly collected to measure the levels of hemagglutination (HI). The removed spleens were fixed with 10% formalin buffer. The specimens were cut in 5-micron diameters and stained with hematoxylin and eosin. Results and Conclusion There was a statistically significant difference in the mean of HI blood titers between the chicks in the growth period and final period groups (p < 0.05). The white-pulp tissue samples were more clearly seen in the treatment group than in the control group, and also, it was observed that the wall of the central artery of the white pulp was thicker in the ginger-treated group as compared with the control group. The nutritional value of ginger may vary. Thus, it is necessary to investigate the effect of this plant final on weight gain; the serum factors associated with the metabolic chart, and the response of the immune system to this plant.

scholarly journals Hepatoprotective effect of galangin on carbon tetrachloride-induced hepatotoxicity via the LKB1/AMPK pathway

2021 ◽  
Vol 19 ◽  
pp. 205873922110008
Author(s):  
Meng Chen ◽  
Xinyan Song ◽  
Jifang Jiang ◽  
Lei Xing ◽  
Pengfei Wang
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Toxicity ◽  
Corn Oil ◽  
Histopathological Examination ◽  
Hepatoprotective Effect ◽  
Control Group ◽  
Group Model ◽  
Protective Effects ◽  
Model Group ◽  
Expression Levels

To investigate the protective effects of galangin on liver toxicity induced by carbon tetrachloride (CCl4) in mice. Mouse hepatotoxicity model was established by intraperitoneal injection (i.p.) of 10 ml/kg body weight CCl4 that diluted with corn oil to a proportion of 1:500 on Kunming mice. The mice were randomly divided into five groups named control group, model group, and 1, 5, and 10 mg/kg galangin group. The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed by ELISA. Liver histopathological examination was observed via optical microscopy. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), and glutathion (GSSG) were analyzed to assess oxidative stress. Finally, western blot assay was carried out to analyse the expression levels of total AMP-activated protein kinase (AMPK), phospho-AMPK (p-AMPK), total liver kinase B1 (LKB1), and phospho-LKB1 (p-LKB1). Compared with the control group, in the model group, the levels of AST, ALT, MDA, and GSSG increased significantly ( p < 0.01); the activity of SOD and GSH decreased significantly ( p < 0.01); and the histopathological examination revealed liver necrosis. However, treatment with galangin (5 and 10 mg/kg) significantly reversed these CCl4-induced liver damage indicators. Furthermore, treatment with galangin (10 mg/kg) significantly increased the p-AMPK and p-LKB1 expression levels ( p < 0.01). This study supports the hepatoprotective effect of galangin against hepatotoxicity, perhaps occurring mainly through the LKB1/AMPK-mediated pathway.

scholarly journals Probucol Attenuates Cyclophosphamide-induced Oxidative Apoptosis, p53 and Bax Signal Expression in Rat Cardiac Tissues

2010 ◽  
Vol 3 (5) ◽  
pp. 308-316 ◽  
Author(s):  
Yousif A. Asiri
Keyword(s):  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Mrna Expression ◽  
Corn Oil ◽  
Lipid Lowering ◽  
Control Group ◽  
Albino Rats ◽  
Protective Effects ◽  
Antioxidant Genes ◽  
Cardiac Tissues

Cyclophosphamide (CP) is a widely used drug in cancer chemotherapy and immunosuppression, which could cause toxicity of the normal cells due to its toxic metabolites. Probucol, a cholesterol-lowering drug, acts as potential inhibitor of DNA damage and shows to protect against doxorubicin-induced cardiomyopathy by enhancing the endogenous antioxidant system including glutathione peroxidase, catalase and superoxide dismutase. This study examined the possible protective effects of probucol, a lipid-lowering compound with strong antioxidant properties, against CPinduced cardiotoxicity. This objective could be achieved through studying the gene expression-based on the possible protective effects of probucol against CP-induced cardiac failure in rats. Adult male Wistar albino rats were assigned into four treatment groups: Animals in the first (control) and second (probucol) groups were injected intraperitoneally with corn oil and probucol (61 mg/kg/day), respectively, for two weeks. Animals in the third (CP) and fourth (probucol plus CP) groups were injected with the same doses of corn oil and probucol (61 mg/kg/day), respectively, for one week before and one week after a single dose of CP (200 mg/kg, I.P.). The p53, Bax, Bcl2 and oxidative genes signal expression were measured by real time PCR. CP-induced cardiotoxicity was clearly observed by a significant increase in serum creatine phosphokinase isoenzyme (CK-MB) (117%), lactate dehydrogenase (LDH) (64%), free (69%) and esterified cholesterol (42%) and triglyceride (69%) compared to control group. In cardiac tissues, CP significantly increases the mRNA expression levels of apoptotic genes, p53 with two-fold and Bax with 1.6-fold, and decreases the anti-apoptotic gene Bcl2 with 0.5-fold. Moreover, CP caused downregulation of antioxidant genes, glutathione peroxidase, catalase, and superoxide dismutase and increased the lipid peroxidation and decreased adenosine triphosphate (ATP) (40%) and ATP/ADP (44%) in cardiac tissues. Probucol pretreatment not only counteracted significantly the CP-induced increase in cardiac enzymes and apoptosis but also induced a significant increase in mRNA expression of antioxidant enzymes and improved ATP, ATP/ADP, glutathione (GSH) in cardiac tissues. In conclusion, data from the present study suggest that probucol prevents the development of CP-induced cardiotoxicity by a mechanism related, at least in part, to its ability to increase mRNA expression of antioxidant genes and to decrease apoptosis in cardiac tissues with the consequent improvement in mitochondrial oxidative phosphorylation and energy production.

scholarly journals The Effect of Zinc and Melatonin Supplementation on Lipid Peroxidation of Various Tissues of Rats with by DMBA-Induced Breast Cancer

2020 ◽  
Vol 11 (1) ◽  
pp. 7580-7588
Keyword(s):  
Breast Cancer ◽  
Lipid Peroxidation ◽  
Kidney Tissue ◽  
Female Rats ◽  
Control Group ◽  
Tissue Samples ◽  
Cancer Group ◽  
Group 5 ◽  
Group 2 ◽  
Group Control Group

The purpose of this study was to investigate the effects of zinc and melatonin administration on lipid peroxidation in various tissues in DMBA-induced breast cancer in female rats. A total of 42 recently weaned Wistar rats were divided into 5 groups in the study: Group 1 (Control), Group 2 (DMBA Control), Group 3 (DMBA+Zinc), Group 4 (DMBA+Melatonin), Group 5 (DMBA+Melatonin, and Zinc). MDA (malondialdehyde) and GSH (glutathione) levels were determined via the spectrophotometric method in the lung, liver, spleen, pancreas, and kidney tissue samples taken from experimental animals. The highest lung, liver, spleen, pancreas, and kidney tissue MDA levels were obtained in the DMBA-induced breast cancer group control group (G2) (p<0.05). MDA levels in DMBA+Zinc (G3), DMBA+Melatonin (G4), and DMBA+Melatonin and Zinc (G5) were significantly lower than group 2 (p<0.05). Similarly, lung, liver, spleen, pancreas, and kidney tissue GSH levels of DMBA+Zinc (G3), DMBA+Melatonin (G4), and DMBA+Melatonin and Zinc (G5) were significantly higher than that of Group 2 (p<0.05). The findings of the study indicated that increased lung, liver, spleen, pancreas, and kidney damage in DMBA-induced breast cancer is suppressed with the supplementation of zinc, melatonin, and combined zinc and melatonin.

Ameliorative Effects of Quercetin in Cyclophosphamide-Induced Vascular Toxicity in Rats

2021 ◽  
Author(s):  
EMİN ŞENGÜL ◽  
VOLKAN GELEN ◽  
SEMİN GEDİKLİ ◽  
ELİF ERBAS ◽  
ASLIHAN ATASEVER
Keyword(s):  
Superoxide Dismutase ◽  
Single Dose ◽  
Corn Oil ◽  
Endothelial Damage ◽  
Control Group ◽  
High Dose ◽  
Protective Effects ◽  
Vascular Toxicity ◽  
Relaxation Responses

Abstract Cyclophosphamide (CYP) causes vascular toxicity and endothelial damage. In this study aimed the determination of the protective effects of Quercetin (Q) in the CYP-induced vascular toxicity in rats. The rats were randomly divided into the following five groups: Control, CYP, Q50+CYP, Q100+CYP and Q100. The control group was given intragastric (i.g.) corn oil for seven days. The CYP group received i.g. corn oil for seven days and a single dose (200 mg/kg) of CYP via intraperitoneal (i.p.) injection on the seventh day. The rats in the three Q-treated groups received Q for seven days. On the seventh day after the Q treatment, the Q50+CYP, and Q100+CYP groups were injected to single dose (200 mg/kg, i.p.) of CYP. The CYP-treatment both worsen the Phenylephrine (PE)-induced contractions and acetylcholine (ACh)-induced relaxation responses in isolated thoracic aorta of rats, and the application of Q corrected these responses. The malondialdehyde (MDA) levels were significantly higher in the CYP-treated groups. The both dose of Q decreased the MDA level. Superoxide dismutase (SOD) and glutathione (GSH) activities were significantly decreased in the CYP group, whereas the high dose of Q increased SOD and GSH activities. Q treatment attenuated CYP-induced pathologies, and endothelial damage. According to results, Q has protective effects against CYP-induced vascular toxicity in rats.

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