Cadmium Toxicity In Rats Research Articles

Naringenin Against Cadmium Toxicity in Fibroblast Cells: An Integrated Network Pharmacology and In Vitro Metabolomics Approach.

Cadmium, a heavy metal, disrupts cellular homeostasis and is highly toxic, with no effective treatments currently available against its toxicity. According to studies, phytochemicals provide a promising strategy for mitigating cadmium toxicity. Naringenin (NG), a potent antioxidant found primarily in citrus fruits, showed protective properties against cadmium toxicity in rats. Nonetheless, the precise mechanism of cadmium cytotoxicity in fibroblasts remains unknown. This study evaluated NG against cadmium (CdCl2) toxicity utilizing network pharmacology and in silico molecular docking, and was further validated experimentally in rat fibroblast F111 cells. Using network pharmacology, 25 possible targets, including the top 10 targets of NG against cadmium, were identified. Molecular docking of interleukin 6 (IL6), the top potential target with NG, showed robust binding with an inhibition constant (Ki) of 58.76 μM, supporting its potential therapeutic potential. Pathway enrichment analysis suggested that "response to reactive oxygen species" and "negative regulation of small molecules metabolic process" were the topmost pathways targeted by NG against cadmium. In vitro analysis showed that NG (10 μM) attenuated CdCl2-induced oxidative stress by reducing altered intracellular ROS, mitochondrial mass, and membrane potential. Also, NG reversed CdCl2-mediated nuclear damage, G2/M phase arrest, and apoptosis. GC/MS-based metabolomics of F111 cells revealed CdCl2 reduced cholesterol levels, which led to alterations in primary bile acid, steroid and steroid hormone biosynthesis pathways, whereas, NG restored these alterations. In summary, combined in silico and in vitro analysis suggested that NG protected cells from CdCl2 toxicity by mitigating oxidative stress and metabolic pathway alterations, providing a comprehensive understanding of its protective mechanisms against cadmium-induced toxicity.

Protection of probiotic Bacillus coagulans and Lactobacillus plantarum against cadmium toxicity in rats

Protection of probiotic Bacillus coagulans and Lactobacillus plantarum against cadmium toxicity in rats

The effect of Ulva rigida (C. Agardh, 1823) against cadmium-induced apoptosis and oxidative stress

Abstract Cadmium (Cd) is known as a pollutant source in recent years with the increase in industrialization. Algae have secondary metabolites with high biological activity, used for pharmaceutical agents. The liver and kidney are the primary organs involved in the elimination of systemic cadmium and the main targets of cadmium toxicity. In the previous research, it was determined the ameliorative effects of the extract obtained from Ulva rigida in the liver tissue of rats induced by cadmium. 35 female Wistar rats between 225-240 g were used. The subjects were injected subcutaneously with 1 mg/kg cadmium chloride (CdCl2) four times a week for four weeks. The study was carried out by groups as control (G1), Cadmium group (1 mg/kg CdCl2-G2), Algae group (100 mg/kg-G3), Cd+algae group (1 mg/kg CdCl2+50 mg/kg algae extract-G4) and Cd+algae group (1 mg/kg CdCl2+100 mg/kg algae extract -G5). The subjects were sacrificed by cervical dislocation. Liver tissue and cardiac blood were collected. It was determined that oxidative stress with iNOS, inflammation and apoptosis with TNF-α increased with cadmium induction, while there was a statistically significant decrease in the groups that were given algae extract. In addition, biochemical changes in SOD, CAT and MDA values were found to be significant (p<0.05). As a result, it was determined that algae extract could play a protective role with its antioxidant and antiapoptotic properties in experimentally induced cadmium toxicity in rats.

Protective effect of Vitamin C and E on enzymatic and antioxidant system in liver and kidney toxicity of Cadmium in rats

The present study aimed to evaluate Heavy metals are persistent and uninterrupted ecological pollutants that are capable to cause numerous dysfunctions in target tissues of exposed animals as well as humans. In the present experimental study, 60 male wistar rats were divided into control and experimental groups. CdCl2 + Vitamin C through water + Vitamin E intraperitonially at a dose of mg/Kg B.W/day for 45 days. Finally, Tissue Respiration (TR), Glycolytic, Oxidative, Antioxidant Enzymes and Enzymes and Products measurements. The data were analyzed using SPSS through one way ANOVA test at P < 0.05). In the present study an attempt was made to monitor the impact of Cd-toxicity in the tissues of wistar rats. Enzymes of glycolysis i.e. Phosphorylase ‘a’ and Aldolase were found to significantly be elevated, whereas Kreb's cycle and oxidative enzymes, including SDH and Cytochrome-c-oxidase were found to be significantly inhibited, suggesting the metabolic shift from aerobiosis to anaerobiosis, visualized through increased lactate production at the cellular level. Similarly antioxidant enzymes were also affected during Cd-toxicity, and stimulates the production of ROS, diminishing their structures, prohibition of the roles of antioxidants. The findings from this study showed that a combination of Vitamin C&E enhances the biological recovery induced by Cd, pretreatment with antioxidants including Vitamin C&E decreases the oxidative stress, inhibits progressive fluctuations convinced through Cd, repaired the biochemical alterations and reverted to almost normal metabolic regimes. So, nutrient supplements, which are enriched with natural antioxidants should be provided to overcome xenobiotic toxic stress.

Histopathological Findings of Testicular Tissue Following Cadmium Toxicity in Rats

Background & Objective: Reproductive toxicity of cadmium (Cd) as an environmental toxicant has been proved in animals and humans. Exposure to Cd impairs testes organs and can reduce male fertility. The present study was designed to investigate the spectrum of histopathological changes in testicular tissue focusing on Sertoli cells in rats following Cd intoxication.Methods: In the present experiment, acute testicular toxicity was induced by an intraperitoneal injection of 1.2 mg/kg CdCl2 to the animals in the test group, while the control group received normal saline. After 52 days, the animals were euthanized, and testicular tissue was stained by Hematoxylin and Eosin. In addition, immunohistochemical staining was performed on Sertoli cells for Wilms' Tumor, Melan-A, and CD99 to evaluate histopathological changes.Results: Cd caused significant alterations in seminiferous tubules with varying effects on the patterns of spermatozoa production. These histopathological changes were significantly higher in the Cd group, compared to the control group.Conclusion: The Cd-induced stepwise spectrum changes included sloughing, disorganization, hypospermatogenesis, spermatic cell arrest, germ cell hypoplasia, Sertoli cell-only pattern, fibro-hyalinized seminiferous tubules, and calcification. Sertoli cells accumulated and created multinucleated giant cells in the seminiferous tubules during the atrophic process, which could be dependent upon Sertoli cells viability and function.

Protective Effect of Combined Long Time Administration of Selenium and Vitamin C on Liver and Kidney Toxicity of Cadmium in Rats.

Background & Objective:Increased industrial activities leads to prolonged human exposure to industrial pollutant such as cadmium (Cd). ‍Chronic exposure to Cd in Mammals and also human being, can cause damages to various organs and particularly kidneys and liver. The goal of this study was to investigate the prophylactic effects of combined selenium (Se) and ascorbic acid supplement in rat cadmium toxicity.Methods:Sixty adult male Wistar rats were divided to 10 groups: one control, one sham and two clusters of 4 intervention groups which were fed with 1 or 5 mg Cd /kg water, for 28 days. Ascorbic acid supplement was added to drinking water of four groups (10 mg/L). Four groups received intraperitoneal Se (1 mg/kg) at day 1, 5, 10, 15, 20 and 25. Finally, Cd concentration was measured by atomic absorption spectrophotometry in liver and kidney sections. Furthermore, pathological changes were investigated in these sections.Results:The results showed weight gain in Cd groups which received ascorbic acid and Se, in contrast to weight loss in parallel groups without vitamin C and Se. The stronger necrosis and inflammation have been observed in group received 5 mg/kg Cd compared to group with 1 mg/kg Cd (P<0.05). In addition, cadmium level was higher in untreated groups without any supplements, significantly (P<0.05). Conclusion:Drinking water with ascorbic acid may have prophylactic effects across cadmium, and combination of Se and ascorbic acid are associated with higher prophylactic effects in both kidney and liver in rats to decrease the Cd toxicity.

Histopathological Findings of Testicular Tissue Following Cadmium Toxicity in Rats.

Background & Objective:Reproductive toxicity of cadmium (Cd) as an environmental toxicant has been proved in animals and humans. Exposure to Cd impairs testes organs and can reduce male fertility. The present study was designed to investigate the spectrum of histopathological changes in testicular tissue focusing on Sertoli cells in rats following Cd intoxication.Methods:In the present experiment, acute testicular toxicity was induced by an intraperitoneal injection of 1.2 mg/kg CdCl2 to the animals in the test group, while the control group received normal saline. After 52 days, the animals were euthanized, and testicular tissue was stained by Hematoxylin and Eosin. In addition, immunohistochemical staining was performed on Sertoli cells for Wilms' Tumor, Melan-A, and CD99 to evaluate histopathological changes.Results:Cd caused significant alterations in seminiferous tubules with varying effects on the patterns of spermatozoa production. These histopathological changes were significantly higher in the Cd group, compared to the control group. Conclusion:The Cd-induced stepwise spectrum changes included sloughing, disorganization, hypospermatogenesis, spermatic cell arrest, germ cell hypoplasia, Sertoli cell-only pattern, fibro-hyalinized seminiferous tubules, and calcification. Sertoli cells accumulated and created multinucleated giant cells in the seminiferous tubules during the atrophic process, which could be dependent upon Sertoli cells viability and function.

Chronic cadmium toxicity in rats: Treatment with combined administration of vitamins, amino acids, antioxidants and essential metals

The present study was designed to investigate the protective effect of dietary nutrients against cadmium-induced hepatic and renal toxicities in male albino rats. The animals were randomly divided into eleven groups where the control group (Group I) received physiological saline (p.o.) and Group II was administered with cadmium chloride (2 mg/kg, s.c.) only. Groups III, IV, V, VI, VII, VIII and IX received 10 mg/kg dietary nutrients, i.e. thiamine, methionine, N-acetylcysteine (NAC), melatonin, zinc (Zn), vitamin E and cystine, respectively. Group X received a dose of 0.1 mg/kg of selenium (Se) and Group XI was administered with a combination of NAC, Zn, vitamin B1 and melatonin. All treatments were administered orally for 21 days with a concomitant subcutaneous (s.c.) cadmium treatment. Cadmium-intoxicated rats exhibited hepatic and renal toxicities as indicated by elevation of lipid peroxidation and marked decline in superoxide dismutase, glutathione peroxidase, alkaline phosphatase activities and total protein. However, a combined treatment with dietary nutrients, i.e. methionine, zinc, vitamin B1 and N-acetylcysteine ameliorated cadmium-induced lipid peroxidation and oxidative stress as they provoked the antioxidant defense system more significantly, when compared to each of them alone and hence is suggested as protective against cadmium-induced hepatic and renal toxicities.

Hepato-Renal protective Effects of Egyptian Purslane Extract against Experimental Cadmium Toxicity in Rats with Special Emphasis on the Functional and Histopathological Changes.

The study was designed to clarify the hapato-nephroprotective effects of purslane ethanolic extract (PEE) against cadmium toxicity. Cadmium (Cd) is a toxic heavy metal. Cd occurs as environmental and food/ feed contamination causing public and animals health hazards. Liver and kidney are the main target organs for acute and chronic cadmium toxicity. Portulaca oleracea is rich in several vitamins, minerals, antioxidant components, and omega-3 fatty acids mainly α-linolenic acid and eicosapentaenoic acid. Results showed significant elevation of the liver and kidney functions, lipid profile and lipid peroxidation. In contrast to the antioxidants enzymatic were greatly decreased. The hepatic and renal tissues showed severe degeneration and necrosis accompanied by severe congestion and multifocal hemorrhages in Cd intoxicated rats. All parameters and tissues showed no changes in rates-treated with both Cd and purslane extract as compared with the control rats. The administration of PEE provided a significantly protection against Cd-induced hepato-nephrotoxicity.

Propolis alcohol extract attenuates prostate specific antigen disorders and prostate necrosis induced by the cadmium toxicity in rats

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Propolis alcohol extract attenuates prostate specific antigen disorders and prostate necrosis induced by the cadmium toxicity in rats

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Protective effects of synbiotic diets of Bacillus coagulans, Lactobacillus plantarum and inulin against acute cadmium toxicity in rats

BackgroundCadmium is a heavy metal that causes oxidative stress and has toxic effects in humans. The aim of this study was to investigate the influence of two probiotics along with a prebiotic in preventing the toxic effects of cadmium in rats.MethodsTwenty-four male Wistar rats were randomly divided into four groups namely control, cadmium only, cadmium along with Lactobacillus plantarum (1 × 109 CFU/day) and inulin (5% of feedstuff) and cadmium along with Bacillus coagulans (1 × 109 spore/day) and inulin (5% of feedstuff). Cadmium treated groups received 200 μg/rat/day CdCl2 administered by gavage. During the 42-day experimental period, they were weighed weekly. For evaluation of changes in oxidative stress, the levels of some biochemicals and enzymes of serum including SOD, GPX, MDA, AST, ALT, total bilirubin, BUN and creatinine, and also SOD level of livers were measured at day 21 and 42 of treatment. The cadmium content of kidney and liver was determined by using atomic absorption mass spectrophotometry. Data were analyzed using analysis of variance (ANOVA) followed by Duncan’s post hoc test.ResultsTreatment of cadmium induced rats with synbiotic diets significantly improved the liver enzymes and biochemical parameters that decreased AST, ALT, total bilirubin, BUN and metal accumulation in the liver and kidney and increased body weight, serum and liver SOD values in comparison with the cadmium-treated group. No significant differences were observed with MDA and GPX values between all groups (p > 0.05).ConclusionsThis study showed that synbiotic diets containing probiotics (L. plantarum and B. coagulans) in combination with the prebiotic (inulin) can reduce the level of cadmium in the liver and kidney, preventing their damage and recover antioxidant enzymes in acute cadmium poisoning in rat.

The Protective Effects of Probiotic Bacteria on Cadmium Toxicity in Rats.

One of the useful properties of probiotic bacteria is their capacity to bind different targets, thus eliminating them through feces. It is supposed that one of these targets could be cadmium, a widespread environmental toxicant that causes various disturbances in biological systems. This study examined the protective effects of probiotic supplementation against cadmium-induced toxicity in the rat. The experiment was conducted in the course of 5 weeks. Animals were divided into four groups: (1) controls, (2) probiotics treated, (3) cadmium treated, and (4) probiotics + cadmium treated. The cadmium concentration was measured in the blood, liver, kidney, and feces, as well as the blood alanine aminotransferase (ALT) and aspartate aminotransferase (AST) as biomarkers of the liver function. Histomorphological changes in the liver and kidney were also determined. Our results revealed that probiotics combined with cadmium increase this metal concentration in feces. As a result, blood, liver, and kidney Cd levels, as well as blood ALT and AST activities were lessened compared to the rat group treated with cadmium only. Besides, probiotics consumed simultaneously with cadmium attenuated histomorphological changes in the liver and kidney caused by cadmium. The rise in lactobacilli number in feces of rats treated simultaneously with cadmium and probiotics results in strong correlation with the increase of Cd concentration in their feces and the decrease of Cd concentration in their blood. We speculate that probiotics actively contribute to cadmium excretion through feces, probably, by its binding to their bacterial cell wall.

Hepatoprotective activity of Moringa oleifera against cadmium toxicity in rats.

Aim:The present investigation has been conducted to evaluate the hepatoprotective activity of Moringa oleifera against cadmium-induced toxicity in rats.Materials and Methods:For this study, 18 Wistar albino rats were taken. Control group, Group I rats were given cadmium chloride @ 200 ppm per kg and Group II rats were treated with M. oleifera extract @ 500 mg/kg along with cadmium chloride @ 200 ppm per kg (daily oral for 28 days). On 29th day, animals were slaughtered and various parameters were determined. Serum biomarkers, oxidative stress parameters, histomorphological examination were carried out with estimation of cadmium concentration in liver tissues.Results:Oral administration of cadmium chloride @ 200 ppm/kg for 28 days resulted in a significant increase in aspartate aminotransferase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), significant (p≤0.01) increase of lipid peroxidation (LPO) and decrease in superoxide dismutase (SOD), and increase in cadmium accumulation in liver. Treatment with M. oleifera @ 500 mg/kg significantly (p<0.01) decreased the elevated ALP, AST, ALT, LPO levels and increase in SOD levels, and as compared to cadmium chloride treated group. However, there was no significant difference in cadmium concentration in liver when compared with cadmium chloride treated group.Conclusion:The study conclude that supplementation of M. oleifera (500 mg/kg), daily oral for 28 days has shown protection against cadmium-induced hepatotoxicity.

A new cytotoxic ceramide from Heteroxenia ghardaqensis and protective effect of chloroform extract against cadmium toxicity in rats

A new ceramide 2S,3R-4E,8E-2-(hexadecanoylamino)-docosa-4,8-diene-1,3-diol (1), along with two known ceramides, namely, 2S,3R-4E,8E-2-(octadecanoylamino)-octadeca-4,8-diene-1,3-diol (2) and 2S,3R-4E-2-(octadecanoylamino)-octadec-4-ene-1-ol (3) were isolated from the chloroform extract of the Egyptian Red Sea soft coral Heteroxenia ghardaqensis. Additionally, cholesterol, cholesterol-3β-acetate, 7β-hydroxy cholesterol, cosanyl octadecanoate, and hexadecanyl octadecanoate were also isolated. The isolated compounds were identified by spectroscopic methods involving 1D, 2D-NMR and ESI-MS. The ceramides (1) and (2) showed moderate cytotoxic activity as growth inhibitors of human hept-G2 cancer cell lines. The protective action of the chloroform extract on cadmium-induced adrenal toxicity was observed by the decrease of the hydropic degeneration in the cortex and normal medulla.

Sexual dimorphism of cadmium-induced toxicity in rats: involvement of sex hormones

The toxic effect of cadmium varies with sex in experimental animals. Previous studies have demonstrated that pretreatment of male Fischer 344 (F344) rats with the female sex hormone progesterone markedly enhances the susceptibility to cadmium, suggesting a role for progesterone in the sexual dimorphism of cadmium toxicity. In the present study, we attempted to further elucidate the mechanism for sex differences in cadmium-induced toxicity in F344 rats. A single exposure to cadmium (5.0 mg Cd/kg, sc) was lethal in 10/10 (100 %) female compared with 6/10 (60 %) male rats. Using a lower dose of cadmium (3.0 mg Cd/kg), circulating alanine aminotransferase activity, indicative of hepatotoxicity, was highly elevated in the cadmium treated females but not in males. However, no gender-based differences occurred in the hepatic cadmium accumulation, metallothionein or glutathione levels. When cadmium (5.0 mg Cd/kg) was administered to young rats at 5 weeks of age, the sex-related difference in lethality was minimal. Furthermore, although ovariectomy blocked cadmium-induced lethality, the lethal effects of the metal were restored by pretreatment with progesterone (40 mg/kg, sc, 7 consecutive days) or β-estradiol (200 μg/kg, sc, 7 consecutive days) to ovariectomized rats. These results provide further evidence that female sex hormones such as progesterone and β-estradiol are involved in the sexual dimorphism of cadmium toxicity in rats.

Influence of N-acetylcysteine on renal toxicity of cadmium in rats

The aim of this study was to investigate the ability of N-acetylcysteine (NAC) to prevent cadmium (Cd)-induced renal damage and whether NAC would reverse cadmium damage to the kidney. Fifty adult male rats were divided into five experimental groups: group 1 received tap water for 3 months and 7 days, group 2 received cadmium chloride (CdCl(2)) for 3 months, group 3 (NAC cotreatment group) received CdCl(2) and 0.5% NAC in tap water for 3 months, group 4 received CdCl(2) in tap water for 3 months and 3 months later received only tap water for 7 days, and group 5 (NAC posttreatment group) received CdCl(2) in tap water for 3 months and 3 months later received 2% NAC in tap water for 7 days. NAC significantly decreased the elevated kidney malondialdehyde levels, as a marker of lipid peroxidation, in both cotreatment and posttreatment modalities. Cotreatment and posttreatment with NAC significantly increased kidney superoxide dismutase enzyme activity and glutathione level but did not change kidney catalase enzyme activity. NAC decreased fractional excretion of sodium in posttreatment group. Neither Cd nor NAC affected the glomerular filtration rate (GFR). Cotreatment and posttreatment with NAC reduced the effects of Cd on proximal tubules. It was found that NAC showed these effects without changing kidney accumulation of cadmium. Exogenously administrated NAC might reduce toxic effects of Cd on the kidney without any reduction in tissue Cd level.

The hepatoprotective effects of selenium against cadmium toxicity in rats

Exposure to cadmium and other pollutants is a major environmental problem. Cadmium is causing acute liver injury but the mechanism of hepatotoxicity is poorly understood. The present study aimed to assess the possible reasons by which cadmium causes liver toxicity. Furthermore, the protective role of selenium against this toxicity was investigated. The hepatic level of lipid peroxidation (malondialdehyde, MDA), the antioxidant system (reduced glutathione, glutathione peroxidase, and thioredoxin reductase), as well as the levels of different lipid classes and the fatty acids pattern were determined in three groups of rats of 15 each. The first group (control group) received saline solution intraperitoneal (i.p.) daily for 10 days. The second group (cadmium chloride-treated group) received 2 mg/kg body weight cadmium chloride solution i.p. for a period of 10 days. The third group (cadmium chloride/sodium selenite-treated group) received cadmium chloride as in the second group and received i.p. sodium selenite (1 mg/kg body weight) at the first and sixth day of treatment (two separate injections within 10 days). The results showed that cadmium treatment increased the hepatic level of malondialdehyde (MDA) and the mean percent of total saturated fatty acid in all lipid classes, whereas the levels of antioxidant system, the levels of hepatic cholesterol esters, triglycerides, total phospholipids, mono- and polyunsaturated fatty acids in all lipid classes were decreased compared to control rats. These changes resulting from Cd-treatment were prevented due to treatment of rats with selenium since the levels of reduced glutathione, glutathione peroxidase, and thioredoxin reductase were induced in Se/Cd-treated group compared with either Cd-treated or control group. In addition, selenium maintained the low levels of cholesterol esters, triglycerides, total phospholipids, mono- and polyunsaturated fatty acids in all lipid classes caused by cadmium to their normal levels. It is concluded that cadmium-induced oxidative stress by increasing the levels of free radicals and by decreasing antioxidants level. This oxidative stress could be the primary cause of Cd-induced hepatotoxicity. Also, selenium can be used as a protective agent against Cd-toxicity. This study could provide a possible explanation to hepatotoxicity resulting from exposure to cadmium in the environment. In addition, selenium could ameliorate cadmium-induced hepatotoxicity since it reduced MDA levels and increased the activities of antioxidant enzymes in this tissue.

Influence of antioxidants on metallothionein-mediated protection in cadmium-fed rats.

Reduced glutathione (GSH) and alpha-tocopherol offer significant protection against cadmium toxicity in rats. They mobilize cadmium from soft tissues like the liver and kidney, but not from the testis. They diminish oxidative stress by raising GSH and reducing lipid peroxidation. However, no further induction of metallothionein (MT) was observed on their treatment to cadmium-fed rats, with the exception of the kidney in the cadmium- and GSH-treated group. Involvement of regulatory domains (viz. metal responsive elements and metal transcription factor) has also been discussed. It is concluded that MT and antioxidants employ different mechanisms of protection. Genes maintaining the intracellular level of GSH seem to control the entire process of protection by these antioxidants.

Effect of taurine on toxicity of cadmium in rats

A study was undertaken to investigate the effect of taurine on the toxicity of cadmium in male Wistar rats. The rats were divided into six groups and fed different diets with or without supplement of 5% taurine and 150–300 ppm cadmium for 2 months. It was found that the body weight of rats, the ratios of liver and kidney weight to body weight, and the level of glutathione in the liver were decreased with increasing the dose of cadmium. The levels of cadmium in the liver and kidney, the levels of thiobarbituric acid-relative substances (TBARS) in the plasma and liver, the activities of aspartate transaminase (AST) and alanine transaminase (ALT) in the plasma, and the levels of blood urea nitrogen (BUN) and creatinine in the plasma of rats were increased with the increasing dose of cadmium. Hence, symptoms of cadmium toxicity in rats included loss of body weight, hepatotoxicity and nephrotoxicity. However, these toxic effects of cadmium were significantly reduced when the rats fed diet with supplement of taurine. Furthermore, the level of cadmium in the feces of rats treated with taurine and cadmium was higher than that of rats treated with cadmium alone. It indicated that taurine might play a role in reducing the toxic effect of cadmium in rats.