Effects of Chronic Cadmium Poisoning on Zn, Cu, Fe, Ca, and Metallothionein in Liver and Kidney of Rats

An experiment was conducted to invest effects of chronic cadmium poisoning on Zn, Cu, Fe, Ca, and metallothionein gene expression and protein synthesis in liver and kidney in rats. Forty rats, 6?weeks old, were randomly allocated into two groups. A group was given CdCl(2) (1?mg/KgCd(2+)) by intraperitoneal injection once a day. The other group was treated with normal saline in the same way. Liver and kidney were collected for analysis at the end of the third week. Results showed that Cd exposure increased Cd (P?相似文献   

On metallothionein,cadmium, copper and zinc relationships in the liver and kidney of adult rats

1. A short-term exposure of adult Wistar rats to Cu (50 μg/ml) and Cd (10.0 μg/ml drinking water) caused significant changes in the subcellular concentrations of Cd, Cu, Zn and metallothionein (MT) in the liver and kidney; the concentrations were close to the physiological values, however.2. To establish a relationship between these changes in the subcellular concentrations of Cd, Cu, Zn and the level of MT in the post-mitochondrial fraction of the liver and kidney, the analytical data (N = 42) were subjected to the multiple regression analysis.3. The analysis showed that MT synthesis in the liver was principally induced by small amounts of Cd (0.32–1.4 μg/g wet wt) whereas in the kidney a level of MT in the post-mitochondrial fraction correlated positively with the renal Cd and Cu, as well as with the level of this protein in the liver.4. The above results together with the positive correlation between the level of MT in the post-mitochondrial fraction and the concentration of Cu in this fraction, as well as the fact that under normal physiological conditions the capacity of MT (β-domain) in the liver and kidney was sufficient to bind 50–100% of the total post-mitochondrial Cu suggest that MT, first induced by small amounts of Cd, may be involved in the metabolism of Cu.     

Metallothionein levels in willow ptarmigan (<Emphasis Type="Italic">Lagopus lagopus</Emphasis>) populations with different natural loads of cadmium

The tissues of willow ptarmigan in some Norwegian mountain areas contain elevated concentrations of cadmium (Cd). It is not known whether such high Cd levels would have negative impacts in otherwise healthy populations of this species. The aim of the current study was to clarify relationships between hepatic and renal metallothionein (MT) and Cd concentrations in willow ptarmigan to assess effects from this metal. The study reported here was undertaken on willow ptarmigan from the Kongsvoll area, with a naturally high Cd load, and the Essand area, with a naturally low Cd load. Cd values in liver and kidney in willow ptarmigan from Kongsvoll were significantly higher than in willow ptarmigan from Essand. The MT content in both tissues was also highest in willow ptarmigan from Kongsvoll. The MT concentration in kidney was twice that in liver for ptarmigan from both areas and at all times of the year. The MT level in both liver and kidney varied greatly throughout the season, with the highest content in spring (May). The variation was greatest in liver. The total material showed a significant linear relationship between Cd and MT levels in both liver and kidney, but a breakdown of the material into seasons and areas gave a varying degree of significance. MT in willow ptarmigan may be an important mechanism for detoxifying Cd, and populations exposed to high load may “respond” to the loads by increasing MT synthesis in tissues such as liver and kidney. There is no evidence that willow ptarmigan from areas with high natural Cd loads have reached a limit for MT synthesis in either liver or kidney.     

Effects of copper, cadmium and chromium cations on the freshwater fish Clarias batrachus L

The data on the effects of cations such as Cu2+, Cd2+ and Cr6+ on the changes in the biochemical parameters in a freshwater fish, Clarias batrachus L., showed an increase of the protein content in the liver, kidney, stomach, intestine, testis and ovary, and a decrease in the muscle after Cu2+ and Cd2+ treatment as compared with control data; but the Cr6+ did not cause any changes of protein concentration in the kidney and testis. The administration of Cu2+ and Cd2+ increased the concentration of free amino acids in all the fish organs, whereas the Cr6+ did not changes this concentration in the muscle. A decrease in dry weight, and an increase in tissue permeability after these treatments were recorded in all the organs studied. In general, the above biochemical parameters of the organs were affected by treatments of the above cations in the following order: Cd greater than Cu greater than Cr over control values of C. batrachus, and their effects were markedly pronounced in the liver and kidney, followed by the intestine, stomach, muscle, testis and ovary in this species.     

Anti-oxidative effect of a protein from Cajanus indicus L against acetaminophen-induced hepato-nephro toxicity

Overdoses of acetaminophen cause hepato-renal oxidative stress. The present study was undertaken to investigate the protective effect of a 43 kDa protein isolated from the herb Cajanus indicus, against acetaminophen-induced hepatic and renal toxicity. Male albino mice were treated with the protein for 4 days (intraperitoneally, 2 mg/kg body wt) prior or post to oral administration of acetaminophen (300 mg/kg body wt) for 2 days. Levels of different marker enzymes (namely, glutamate pyruvate transaminase and alkaline phosphatase), creatinine and blood urea nitrogen were measured in the experimental sera. Intracellular reactive oxygen species production and total antioxidant activity were also determined from acetaminophen and protein treated hepatocytes. Indices of different antioxidant enzymes (namely, superoxide dismutase, catalase, glutathione-S-transferase) as well as lipid peroxidation end-products and glutathione were determined in both liver and kidney homogenates. In addition, Cytochrome P450 activity was also measured from liver microsomes. Finally, histopathological studies were performed from liver sections of control, acetaminophen-treated and protein pre- and post-treated (along with acetaminophen) mice. Administration of acetaminophen increased all the serum markers and creatinine levels in mice sera along with the enhancement of hepatic and renal lipid peroxidation. Besides, application of acetaminophen to hepatocytes increased reactive oxygen species production and reduced the total antioxidant activity of the treated hepatocytes. It also reduced the levels of antioxidant enzymes and cellular reserves of glutathione in liver and kidney. In addition, acetaminophen enhanced the cytochrome P450 activity of liver microsomes. Treatment with the protein significantly reversed these changes to almost normal. Apart from these, histopathological changes also revealed the protective nature of the protein against acetaminophen induced necrotic damage of the liver tissues. Results suggest that the protein protects hepatic and renal tissues against oxidative damages and could be used as an effective protector against acetaminophen induced hepato-nephrotoxicity.     

Coral fossil: A potential adsorbent of natural source for cadmium removal in broilers

Cadmium (Cd) is a pollutant that poses a health risk for humans and animals. Coral fossil (CF) acts as an adsorbent, yet limited knowledge is available on impacts of CF on Cd toxicities. The work was performed to figure out the effects of CF on hematobiochemical details and specific organs in Cd exposed broilers. The experiment was carried out with 45 broilers and were divided into three groups (15 in each). Group A was served as control. The birds in group B received Cd (75 mg /kg b. w.) orally. Whereas group C was orally supplemented with Cd (75 mg /kg b. w.) and CF (1 gm/kg b. w.). The trial was lasted for 30 days. For hematobiochemical analysis, blood samples were drawn, and sera were separated. Liver, kidney and muscle were collected to assess accumulation concentration. Brain, liver and kidney samples were also collected for histopathological study. The results showed that hematological parameters (TEC, Hb, PCV, MCV, MCH, MCHC and DLC) were altered by Cd but restored with CF supplementation. Liver (AST, ALT and ALP) and kidney (total protein and creatinine) biomarkers were increased significantly in Cd treated broilers while decreased significantly after CF supplementation. CF reduced accumulation concentration of Cd in liver, kidney and muscle. Cd intoxicated broilers showed degenerative changes in brain, hyperplastic bile duct and proliferation of renal tubular epithelium with focal degeneration and necrosis; and these were improved after CF supplementation. Therefore, it can be concluded that CF is a potential adsorbent against Cd toxicities.     

Cadmium affects the expression of metallothionein (MT) and glutathione peroxidase (GPX) mRNA in goldfish, Carassius auratus

Cadmium (Cd) is a widespread non-essential heavy metal that enters the aquatic environment as a result of natural and human-caused activities, including industrial effluent, mining, and agricultural runoff. In the present study, we investigated time and dose-related effect of CdCl(2) on metallothionein (MT) and glutathione peroxidase (GPX) mRNA levels in a number of goldfish tissues, in vivo. Basal MT and GPX mRNA levels remained unchanged in the tissues tested throughout the experiment. Injection with CdCl(2) significantly increased MT mRNA levels in the brain, liver, kidney and intestine in a dose-dependant manner at all time tested (6, 12, 24 and 36 h). We isolated the full length GPX cDNA from goldfish kidneys, and found it to contain 785 nucleotides, including an open reading frame, predicted to encode a protein of 142 amino acids. In contrast, injection with CdCl(2) significantly decreased GPX mRNA levels in the liver and kidney in a time-, and dose-, dependant, and became undetectable after 12, 24 and 36 h. The findings provide molecular characterization of MT and GPX in goldfish and suggest that exposure to Cd results in significant physiological changes in goldfish.     

Metallothionein and the development of the mottled disorder in the mouse

Copper accumulates in kidney tissue of mottled (Mo) mice largely in association with a low MW cytosol protein, and the reduced copper levels in neonatal mutant liver are largely the result of a reduction in the amount of copper associated with this same protein. On the basis of ion-exchange chromatographic profile, heat stability, absence of a 280nm absorption peak, and the binding of Cd109 and Zn65 the protein mutants in the kidney is identified as metallothionein (MT). Amino acid analysis, however, failed to confirm this, and it is suggested that the high copper content of the mutant protein results in its oxidative degradation during purification, even when normal anaerobic precautions are taken. Estimates of thionein protein content of tissues from mutant and normal mice demonstrated that the levels are significantly elevated in both young and adult mutant kidney and depressed in young mutant liver, in parallel therefore with the changes in tissue copper levels. In adult mutant liver tissue, however, thionein levels are significantly raised, even though tissue copper content is normal. The synthesis and degradation of MT was examined in some detail. Incorporation of S35-cysteine in kidney MT was significantly raised in both young and adult mutant mice, while in adult tissue the rate of degradation of MT was significantly depressed. The elevated kidney MT levels arise therefore in young mutant mice from an increased rate of synthesis and in adult mice from the combined effects of increased synthesis and reduced degradation.     

Cytoprotective and antioxidant role of diallyl tetrasulfide on cadmium induced renal injury: an in vivo and in vitro study

Cadmium (Cd) is an environmental and industrial pollutant that affects various organs in humans and animals. A body of evidence has accumulated implicating the free radical generation with subsequent oxidative stress in the biochemical and molecular mechanisms of Cd toxicity. Since kidney is the critical target of Cd toxicity, we carried out this study to investigate the effects of diallyl tetrasulfide (DTS), an organosulfur compound derived from garlic on Cd induced toxicity in the kidney of rats and also in the kidney cell line (vero cells). In experimental rats, subcutaneous administration of Cd (3 mg/kg bw/day) for 3 weeks induced renal damage, which was evident from significantly increased levels of serum urea and creatinine with significant decrease in creatinine clearance. A markedly increased levels of lipid peroxidation markers (thiobarbituric acid reactive substances and lipid hydroperoxides) and protein carbonyl contents with significant decrease in nonenzymic antioxidants (total sulphydryl groups, reduced glutathione, vitamin C and vitamin E) and enzymic antioxidants (superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase) as well as glutathione metabolizing enzymes (glutathione reductase, and glucose-6-phosphate dehydrogenase) were also observed in Cd intoxicated rats. Coadministration of DTS (40 mg/kg bw/day) and Cd resulted in the reversal of the kidney function accompanied by a significant decrease in lipid peroxidation and increase in the antioxidant defense system. In vitro studies with vero cells showed that incubation of DTS (5-50 microg/ml) with Cd (10 microM) significantly reduced the cell death induced by Cd. DTS at 40 microg/ml effectively blocked the cell death and lipid peroxidation induced by Cd (10 microM) indicating its cytoprotective property. Further, the flow cytometric assessment on the level of intracellular reactive oxygen species using a fluorescent probe 2', 7'-dichlorofluorescein diacetate (DCF-DA) confirmed the Cd induced intracellular oxidative stress in vero cells, which was significantly suppressed by DTS (40 microg/ml). The histopathological studies in the kidney of rats also showed that DTS (40 mg/kg bw/day) markedly reduced the toxicity of Cd and preserved the architecture of renal tissue. The present study suggests that the cytoprotective potential of DTS in Cd toxicity might be due to its antioxidant and metal chelating properties, which could be useful for achieving optimum effects in Cd induced renal damage.     

Quercetin attenuates lindane induced oxidative stress in wistar rats

A wide number of pesticides, including highly persistent organochlorine compounds, such as lindane (γ-Hexachlorocyclohexane), have deteriorative effect on fauna and flora by inducing oxidative stress. Lindane induces cell damage by producing free radicals and reactive oxygen species. Quercetin, a dietary flavonoid, is ubiquitous in fruits and vegetables and plays an important role in human health by virtue of its antioxidant function. In this study the flavonoid quercetin was used to investigate its antioxidative effect against lindane induced oxidative stress in rats. The level of lipid peroxidation, reduced glutathione (GSH) were analysed in addition to the antioxidant enzymes such as catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD) and glutathione-s-transferase (GST) activities in the liver and kidney tissue. Levels of hepatic marker enzymes in serum like Aspartate transaminase (AST), Alanine transaminase (ALT), Alkaline phosphatase (ALP) and Lactate dehydrogenase (LDH) and renal markers like serum creatinine and serum urea were estimated. Administration of Lindane induced histopathological alterations and increased levels of serum hepatic and renal markers and malondialdehyde (MDA) with a significant decrease in GSH content and CAT, SOD, GPx and GST activities. Cotreatment of quercetin along with lindane significantly decreased the lindane induced alteration in histology, serum hepatic and renal markers and MDA and also improved the cellular antioxidant status. The results show that Quercetin ameliorates Lindane induced oxidative stress in liver and kidney. The quercetin exhibited chemopreventive effect when administered along with lindane.     

Role of alpha-tocopherol in cadmium-induced oxidative stress in Wistar rat's blood, liver and brain

Cadmium (Cd) a highly toxic metal is considered to be a multitarget toxicant, and it accumulates principally in the liver and kidney after absorption. In vivo studies of mouse and rat liver have shown that apoptosis plays a primary role in Cd-induced hepatotoxicity. However, the detailed mechanisms by which toxic metals such as Cd produce their effects are still largely unknown. The present study aimed at investigating the consequences of exposure to Cd, alpha-tocopherol and their combination on stress biochemical parameters (lipoperoxidation and protein carbonyls levels). Male albino Wistar rats (1 month old) were treated intravenously with cadmium (2 mg CdCl(2)/kg body weight/day), and alpha-tocopherol (100 mg/kg body weight/day), or with alpha-tocopherol+Cd (100 mg Vit E/kg body weight, 2 mg CdCl(2)/kg). The lipoperoxidation was measured by the thiobarbituric acid reactive substances (TBARS) method and oxidatively generated damage to proteins by determining carbonyl (DNPH) levels. Among the hematological parameters measured the haematocrit value and haemoglobin concentration were significantly decreased in the blood of Cd-treated rats. A significant increase was observed in the level of malondialdehyde (MDA) and protein carbonyls in the cadmium exposed group compared to control group (p<0.001), and these values were decreased after administration of alpha-tocopherol (group 4). The activity of lactate dehydrogenase in rat liver and brain showed a significant increase as compared to that found in the control group and significant decrease of catalase and superoxide dismutase activities. In the liver of the Cd-treated group the contents of reduced glutathione were decreased. Our results suggest that cadmium induces an oxidation of cellular lipids and proteins and that administration of alpha-tocopherol can reduce Cd-induced oxidative stress and improve the glutathione level together with other biochemical parameters.     

Biomonitoring with the BuzzardButeo buteo in the Netherlands: Heavy metals and sources of variation

The feasibility of using Buzzards found dead as indicators of environmental contamination was tested. Liver, kidney, and tibia specimens were examined for the presence of Cd, Cu, Pb, Mn, and Fe, which were used as markers. All buzzards submitted to the Veterinary Institute in 1992 were examined for cause of death and condition. Results showed that more than half had been poisoned or shot. As the condition of the birds worsened, fat reserves were depleted before protein reserves. Concentrations of the heavy metals rose in liver and kidney as nutrient reserves fell. Since the content of heavy metal per organ was not related to body condition, content was considered a better measure for biomonitoring. The concentrations of Cd, Cu, Pb, Mn, or Fe measured in buzzards were not toxic. In several places buzzards had recently ingested relatively large amounts Cd and/or Pb. Buzzards with high contents of Cd, Cu, Pb, and Mn were found in areas having more than average contamination. The North-South gradient in aerosol deposition and soil content of heavy metals (especially Cd & Pb) was reflected in the Buzzard. We concluded that the Buzzard is a suitable and cost-effective biomonitor, to investigate the bioavailability of ecocontaminants in large areas, to signal gross changes in food webs, and to monitor raptor persecution.     

Cadmium: tissue distribution and binding protein induction in the painted turtle, Chrysemys picta

The freshwater painted turtle, Chrysemys picta, was used to investigate (a) the distribution of an injected dose of ¹⁰⁹Cd in tissues over a period of 192 h (8 days) and (b) the effect of non-isotopic cadmium injection on tissue metal-binding protein levels. Cadmium is cleared from the blood with 9% remaining in the circulation at 192 h. ¹⁰⁹Cd is found in all tissues, but is accumulated preferentially in liver, kidney, pancreas, and gastrointestinal tract. The liver is the primary site of Cd accumulation, accounting for 46.4% of the injected dose by 192 h and the highest Cd concentration (cpm/mg tissue). Steroidogenic tissues and the oviduct accumulate significant amounts of ¹⁰⁹Cd and the isotope is present in yolk. An increase in tissue metal-binding protein level after non-isotopic CdCl₂ injection is consistent with ¹⁰⁹Cd distribution, in that metal-binding protein concentration after CdCl₂ injection is highest in liver, followed by pancreas and kidney with low, but with significant levels of cadmium-binding protein in gonads and steroid target organs. We conclude that the liver is the major site of storage after a single injection of isotopic cadmium and induction of a metal-binding protein may be an adaptive response to exposure to cadmium.     

Cadmium-induced oxidative stress and DNA damage in kidney of pregnant female rats

In the present study, we have investigated the influence of sub-acute treatment with cadmium (Cd) on some parameters indicative of oxidative stress and DNA damage in tissues of pregnant female rats. Pregnant female rats (n=6) were injected subcutaneously, daily with a dose of cadmium chloride of 3 mg/kg body weight (b.w.) from day 6 to day 19 of pregnancy, and they were allowed to deliver normally. MDA level and GPx, CAT and SOD activities were used as markers of oxidative stress in liver and kidney. The 8-oxo-dG level was measured by the HPLC-EC system. Cd treatment increased MDA (+116%, p<0.01) in kidney. Moreover, Cd treatment also decreased CuZn-SOD (-11%, p<0.05) and GSH level (-52%, p<0.05) in kidney. Treated rats displayed an increase of the liver metallothionein (MT) level. Induction of MT in liver was probably implicated in the detoxification of Cd. The high level of Cd (3 mg/kg) used in the present study is partially neutralized by MT in liver, whereas the free fraction could be implicated in the oxidative stress and DNA oxidation observed in kidney. Cd treatment failed to alter 8-oxodGuo, indicating the absence of DNA oxidation in liver; by contrast, the same treatment increased the 8-oxodGuo level (+51%, p<0.05) in the kidney of pregnant female rats, indicating an oxidative stress associated with DNA damage only in kidney.     

Protective effects of azelaic acid against high-fat diet-induced oxidative stress in liver, kidney and heart of C57BL/6J mice

Excess fat intake induces hyperinsulinaemia, increases nutrient uptake and lipid accumulation, amplifies ROS generation, establishes oxidative stress and morphological changes leading to tissue injury in the liver, kidney and heart of high-fat diet (HFD)-fed mice. The effect of azelaic acid (AzA), a C9 α,ω-dicarboxylic acid, against HFD-induced oxidative stress was investigated by assaying the activities and levels of antioxidants and oxidative stress markers in the liver, kidney and heart of C57BL/6J mice. Mice were segregated into two groups, one fed standard diet (NC) and the other fed high-fat diet (HFD) for 15 weeks. HFD-fed mice were subjected to intragastric administration of AzA (80 mg/kg BW)/RSG (10 mg/kg BW) during 11-15 weeks. Glucose, insulin, triglycerides, hepatic and nephritic markers were analysed in the plasma and the activity of enzymatic, non-enzymatic antioxidants and lipid peroxidation markers were examined in the plasma/erythrocytes, liver, kidney and heart of normal and experimental mice. We inferred significant decrease in enzymatic and non-enzymatic antioxidants along with significant increase in glucose, insulin, hepatic and nephritic markers, triglycerides and lipid peroxidation markers in HFD-fed mice. Administration of AzA could positively restore the levels of plasma glucose, insulin, triglycerides, hepatic and nephritic markers to near normal. AzA increased the levels of enzymatic and nonenzymatic antioxidants with significant reduction in the levels of lipid peroxidation markers. Histopathological examination of liver, kidney and heart substantiated these results. Hence, we put forward that AzA could counteract the potential injurious effects of HFD-induced oxidative stress in C57BL/6J mice.     

Comparative effect of water and food-chain mediated cadmium exposure in rats

This study sets out to compare the absorption and toxicity of Cadmium (Cd) administered via the food-chain and inorganic Cd administered in drinking water after 1 and 3 months exposure using rats as animal model. The food-chain was mimicked by exposing rats to diet containing Cd pre-exposed fish. The uptake of Cd by the rats after both mode of exposure was calculated by summing up the Cd burden in the liver and kidneys and was expressed in terms of % intake. The toxicity of Cd was assessed by monitoring biochemical indices of liver function in the plasma and liver. Regardless of the mode of exposure of the rats, the Cd load in the liver and kidney was significantly (P < 0.05) higher than the respective controls with the kidney having a significantly higher load than the liver after both periods of exposure. However irrespective of the mode of exposure, more Cd was accumulated in the liver and kidney of the 3 months exposed rats relative to those exposed for 1 month. The uptake of Cd by rats exposed to Cd via the food-chain for 1 and 3 months was significantly (P < 0.05) lower when compared to the corresponding water mediated Cd exposed rats, except for the liver after 3 months of exposure. The liver l-ALT activity of rats administered inorganic Cd in drinking water for 1 and 3 months was significantly (P < 0.05) lower as compared to controls. Parallel analysis of the plasma showed no significant (P > 0.05) difference in l-ALT activity between both groups after the same periods of exposure. The l-AST activity in the plasma of rats similarly exposed to Cd for 1 and 3 months was significantly (P < 0.05) higher as compared to controls with a corresponding reduction in the liver. Conversely no significant (P > 0.05) change was observed in plasma and liver l-ALT and l-AST activities after food-chain mediated exposure to Cd for 1 and 3 months in relation to their respective controls. These findings indicate that Cd incorporated in fish is more easily bioavailable, but less toxic relative to inorganic Cd salts at the end of 3 months of exposure in rats.     

Cd-, Zn-, Cu-binding protein in the elasmobranch Scyliorhinus canicula

A Cd-, Zn-, Cu-binding protein was isolated from the liver of dogfish subjected to environmental experimental contamination (50 ppm Cd). It was also found in liver from untreated fish. This protein has a high absorption at 250 nm and a low absorption at 280 nm, suggesting a mercaptide bond and a lack of aromatic amino acids. The SDS-PAGE pattern and changes in absorption spectrum on adding Cd or lowering pH are found as for mouse MT. The protein contains Cu and Zn in control and Cu, Zn and Cd in treated fish. Cd levels in the protein are significantly higher in females and significantly increase with treatment duration. Copper levels decrease after 96 hr in males and 6 days in females.     

Analysis of tissue cadmium distribution in chronic cadmium-exposed mice using in-air micro-PIXE

This study undertook the analysis of tissue cadmium (Cd) distribution using in-air micro-particle-induced X-ray emission (PIXE) and the examination of the involvement of metal ions in parenteral Cd toxicity. A mouse was injected intraperitoneally with 3 mg/kg body weight of CdCl₂ thrice weekly. After 27 wk, the liver and kidney were excised and fixed in 10% formalin solution for 4 h and then embedded in paraffin. Thin paraffin sections were used to analyze trace elements with in-air micro-PIXE and to examine metallothionein protein and histological changes. Cd distribution was determined by micro-PIXE in the liver and renal cortex of the Cd-exposed mouse, and the net Cd count was higher in the liver than in the renal cortex. The net iron (Fe) count was higher in the liver of the Cd-exposed mouse compared to the control, and an opposite tendency was observed in the renal cortex. Wide cellular Cd distribution was demonstrated in the liver and renal cortex of the chronic Cd-exposed mouse compared to the control. Metallothionein staining was increased by chronic exposure to Cd both in the liver and kidney, and nephrotoxicity was more apparent than hepatotoxicity. The modification of tissue Fe and calcium distribution by an intraperitoneal injection of Cd might be involved in Cd-induced toxicity.     

The Remedial Efficacy of Spirulina platensis versus Chromium-Induced Nephrotoxicity in Male Sprague-Dawley Rats

This study was conducted to investigate the possible protective effect of Spirulina platensis against chromium-induced nephrotoxicity. A total of 36 adult male Sprague-Dawley rats were divided into 4 equal groups (Gps). Gp1 served as control, rats of Gps 2, 3, and 4 were exposed to Spirulina platensis (300 mg/kg b.wt per os) and sodium dichromate dihydrate (SDD) via drinking water at concentration of 520 mg /l respectively. Chromium administration caused alterations in the renal function markers as evidenced by significant increase of blood urea and creatinine levels accompanied with significant increase in kidney’s chromium residues and MDA level as well as decreased catalase activity and glutathion content in kidney tissue. Histologically, Cr provoked deleterious changes including: vascular congestion, wide spread tubular epithelium necrobiotic changes, atrophy of glomerular tuft and proliferative hyperplasia. The latter was accompanied with positive PCNA expression in kidney tissues as well as DNA ploidy interpretation of major cellular population of degenerated cells, appearance of tetraploid cells, high proliferation index and high DNA index. Morphometrical measurements revealed marked glomerular and tubular lumen alterations. On contrary, spirulina co-treatment with Cr significantly restored the histopathological changes, antioxidants and renal function markers and all the previously mentioned changes as well.