Administration Of Mercuric Chloride Research Articles

Evaluation of Punarnavadi Mandura for haematinic activity against mercuric chloride-induced anemia in albino rats.

Punarnavadi Mandura, a compound Ayurvedic formulation, is one of the most commonly used medicine in the treatment of anemia (Pandu) in Ayurveda. The safety profile of this formulation is well established; however, no pharmacological study has been reported to provide the scientific basis for its use in the treatment of anemia. To evaluate the hematinic effect of Punarnavadi Mandura against mercuric chloride-induced anemia in albino rats. The test drug (Punarnavadi Mandura) was suspended in distilled water and administered orally in a dose of 450 mg/kg for 30 days in rats. Anemia was induced by simultaneous administration of mercuric chloride (9 mg/kg) for 30 consecutive days. Body weight was noted for each animals. At the end, haematological parameters, anaemia markers like serum iron, ferritin, and total iron binding capacity (TIBC), as well as relative weight of organs and histopathology investigation, were examined. Exposure of mercuric chloride to rats for 30 days resulted in a significant decrease of body weight, an increase in the weight of the liver and kidney and a decrease in hemoglobin content. It also decreased serum ferritin to a significant extent and increased serum TIBC. Histopathology of the liver shows macro fatty changes, vacuolization, marked necrosis, and severe degenerative changes, while the kidney shows cell infiltration. All these changes were significantly attenuated by the administration of Punarnavadi Mandura. The present data indicate that Punarnavadi Mandura has possessing marked cytoprotective activity, significantly attenuated the HgCl2-induced adverse changes on red blood cell related parameters, and showing hematinic activity in albino rats.

Antioxidant effects of hydro-alcoholic extract of Ashrasi date palm in hepatotoxicity caused by mercuric chloride administration

Introduction: date palm (ADP) is a flowering plant type of the palm family which has strong antioxidant properties. Mercuric chloride (MC) is a complex substance that generates oxidative stress. This study was designed to investigate the protective effects of ADP on the , inflammatory, oxidative and apoptotic changes induced by MC.
 Methods: Fifty-six male rats were randomly allocated into 8 groups (n = 7) as follows: Group 1- control, 2- MC (50 mg/kg), 3-5: ADP (30, 90, and 270 mg/kg), and 6-8: MC+ADP. The rats were orally and administrated with the respective agents for 5 weeks. Extracts of ADP were prepared and screening was conducted. Nitric oxide (NO), lipid (LP), and Ferric Reducing Ability of Plasma (FRAP) assays were conducted to assess the antioxidant index. The levels of p53, Bcl2 and Bax gene expression were assessed by real-time PCR. Cytokines involved in inflammation were evaluated by enzyme-linked assay (ELISA). Liver enzymes were also measured using biochemical methods. changes (e.g. in hepatocyte (HD) and central hepatic vein (CHV)), and apoptosis cell index were evaluated by light and fluorescent microscopy methods.
 Results: MC treatment significantly increased all parameters described in the Methods section (except for FRAP level and Bcl2 expression level, which were both decreased) in the MC group, when compared to the control group (P < 0.05). Also, all indices were significantly decreased in the ADP and ADP+MC groups (except for FRAP level and Bcl2 expression level, which were increased), when compared to the MC group (P < 0.05).
 Conclusion: These findings revealed that ADP extract can serve as a potent antioxidant which effectively attenuates the adverse effects of MC on the liver through the activation of antioxidant mechanisms and regeneration of modifications.

Effect of Administration of Mercuric Chloride on the Social Behavior, Neuromuscular Coordination, Motor Activity, Blood Parameters and Liver Structure Alterations in Mice Offspring

Effect of Administration of Mercuric Chloride on the Social Behavior, Neuromuscular Coordination, Motor Activity, Blood Parameters and Liver Structure Alterations in Mice Offspring

Hepatoprotective activity of royal jelly on mercuric chloride–induced damage model in rats

Background: Mercuric chloride (MC) is the chemical composition of mercury and chlorine with many side effects such as oxidative stress referring to mercury toxicity. Royal jelly (RJ) as a honey bee secretion has antioxidant activities. This study was designed to evaluate the effects of RJ against the parameters of hepatic damage in male rats induced by MC toxicity. Materials and Methods: In this study, 48 male rats were randomly assigned into six groups: sham (saline) and MC control (50 mg/kg) groups; RJ groups (200 mg/kg RJ for 1 day and 200 mg/kg RJ for 7 days, orally) and MC + RJ groups (200 mg/kg RJ orally + 50 mg/kg MC intraperitoneally for 1 day, and 200 mg/kg RJ orally and 50 mg/kg MC intraperitoneally for 7 days). Griess technique was used for the determination of serum nitric oxide (NO) level. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) concentrations were determined for liver functional disturbances value. In addition, thiobarbituric acid reactive species, antioxidant capacity, the diameter of hepatocytes, and the central hepatic vein (CHV) were investigated. Results: MC administration significantly increased the liver malondialdehyde (MDA) and NO levels, the mean diameter of CHV and hepatocyte, hepatic enzymes, and decreased tissue Ferric reducing antioxidant power (FRAP) level compared to the sham group (P < 0.01). The RJ and RJ + MC in all treatments significantly reduced the mean diameter of hepatocyte and CHV, hepatic enzymes, renal MDA and NO levels, and increased tissue FRAP level compared to the MC control group (P < 0.01). It seems that RJ administration recovers the hepatic injury induced by MC in rats.

Renal toxicity of heavy metals (cadmium and mercury) and their amelioration with ascorbic acid in rabbits

Cadmium and mercury are among the most toxic and dangerous environmental pollutants that may cause fatal implications. Vitamin C is an important chain-breaking antioxidant and enzyme co-factor against heavy metals. The objective of the present study was to evaluate the toxicological effects of cadmium chloride, mercuric chloride, and their co-administration on biochemical parameters of blood serum and metal bioaccumulation in kidneys and also to elucidate the protective effect of vitamin C in rabbits against these metals. In the current research, cadmium chloride (1.5mg/kg), mercuric chloride(1.2mg/kg), and vitamin C (150mg/kg of body weight) were orally administered to eight treatment groups of the rabbits (1, control; 2, vitamin; 3, CdCl2; 4, HgCl2; 5, vitamin + CdCl2; 6, vitamin + HgCl2; 7, CdCl2 + HgCl2, and 8, vitamin + CdCl2 + HgCl2). After the biometric measurements of all experimental rabbits, biochemical parameters viz. creatinine, cystatin C, uric acid, and alkaline phosphatase (ALP) and metal bioaccumulation were determined using commercially available kits and atomic absorption spectrophotometer, respectively. The levels of creatinine (28.3 ± 1.1μmol/l), cystatin C (1932.5 ± 38.5 ηg/ml), uric acid (4.8 ± 0.1mg/day), and ALP (51.6 ± 1.1IU/l) were significantly (P < 0.05) increased due to administration of mercuric chloride but in the presence of vitamin C, the effects of mercuric chloride on creatinine (21.9 ± 1.4μmol/l), cystatin C (1676.2 ± 42.2 ηg/ml), uric acid (3.9 ± 0.1mg/day), and ALP (43.3 ± 0.8IU/l) were less as compared to metal-exposed specimens. Similar results were found in rabbits treated with cadmium chloride and vitamin C and also with co-administration of both metals and vitamin C. Because of the bio-accumulative nature of cadmium chloride and mercuric chloride, these metals were accumulated in kidneys of rabbits, which might lead to deleterious effects. The results of the present study provide an insight into the toxicity of the cadmium chloride, mercuric chloride, and/or their combination on biochemical parameters as well as kidneys of the rabbits and the ameliorating potential of vitamin C against these metals is also evaluated.

Evaluation of Protective Effect of Tageteserecta Against Mercuric Chloride Induced Nephrotoxicity

The toxicity of various forms of mercury to the living organisms is well documented. Mammalian kidney is the main site of decomposition of inorganic mercury as well as the target organ for its toxicity in majority of the animals including human beings. Present study has been aimed to investigate the role of Tageteserecta(family-Astereacea) as a possible modifier of mercury induced renal damages. Experimentation was conducted on one hundred female albino rats, divided into five equal groups, each group again sub-divided into four sub-groups having five rats each: Control group- Orally administrated distilled water only. T. erecta flower extract treated group-10mg/kg b. wt./day for 1, 7, 14, 21 days was administrated orally. Mercuric chloride treatment groups-A dose of 0.926 mg/kg b.wt. for 01 day, 0.132 mg/kg b.wt. for 7 days, 0.066 mg/kg b.wt. for 14 days and 0.044 for 21 days was administrated through oral route. Oral administration of T. erecta flower extract followed by mercuric chloride treatment for 1, 7, 14 and 21 days. Oral administration of Mercuric chloride followed by T. erectaflower extractadministration for 1, 7, 14 and 21 days. These animals were then sacrificed after 1, 7, 14 and 21 days treatment respectively. Controls were also run respectively. Mercuric chloride intoxication resulted in pathological alterations in the kidney of albino rats, such as degradation of glomerulus, proximal and distal tubules. Combined pre and post treatment of T. erectawith mercuric chloride has been found to reduce the pathological alterations in the kidney. Thus, the results from the present study suggest that T. erectacan modify the renal damages against mercuric chloride induced toxicity.

Protective Effect of Origanum Oil on Alterations of Some Trace Elements and Antioxidant Levels Induced by Mercuric Chloride in Male Rats.

In the current study, 48 male rats were classified into four groups (12 rats/group): 1-control group received 1ml distilled water, 2-origanum oil group treated daily with oral dose of origanum oil (5mg/kg) for 30 and 60days, 3-mercuric chloride group treated daily with oral dose of mercuric chloride (4mg/kg) for 30 and 60days, and 4-origanum oil + mercuric chloride group treated with both origanum oil and mercuric chloride (5 and 4mg/kg, respectively) for 30 and 60days. All treatments were carried out by stomach tube. The results showed that administration of mercuric chloride induced significant increase in thiobarbituric acid reactive substance (TBARS) and decrease in glutathione (GSH), catalase (CAT), and super oxide dismutase (SOD) in testis and spleen tissues. The data also showed significant increase in tumor necrossis factor-α (TNF-α), 8-hydroxy deoxyguanosine (8-OHDG), acid phosphatase (ACP), urea, and creatinine. Furthermore, significant decreases in serum zinc (Zn), copper (Cu), magnesium (Mg), iron (Fe), and testosterone in mercuric chloride group were recorded. The histological examination of testis and spleen tissues showed some degenerative changes while significant improvement in the antioxidant levels, biochemical, trace elements, and histological changes were observed in mercuric chloride group treated with origanum oil. It could be concluded that origanum oil through its antioxidant potential may possess health promoting properties and could protect cells from oxidative damage induced by mercuric chloride.

A Vegetable, Launaea taraxacifolia, Mitigated Mercuric Chloride Alteration of the Microanatomy of Rat Brain

ABSTRACTMercuric chloride is an environmental pollutant that affects the nervous systems of mammals. Oxidative damage is one of the mechanisms of its toxicity, and antioxidants should mitigate this effect. A vegetable with antioxidant activity is Launaea taraxacifolia, whose ethanolic extract (EELT) was investigated in this experiment to determine its effect against mercuric chloride (MC) intoxication in rat brain. Thirty male Wistar rats were randomly assigned into five groups (n = 6) as follows: control; propylene glycol; EELT (400 mg/kg bwt) for 19 days; MC (HgCl2) (4 mg/bwt) for 5 days from day 15 of the experiment; EELT+ MC, EELT (400 mg/kg bwt) for 14 days + MC (4 mg/bwt) for 5 days from day 15 of the experiment. All treatments were administered orally by gastric gavage. Behavioral tests were conducted on the 20th day, and rats were euthanized the same day. Blood and brain tissue were examined with regard to microanatomical parameters. Data were analyzed using analysis of variance with statistical significance set at p < .05. MC induced significant (19%) reduction of thrombocytes, which was ameliorated by 57% (p < .05) by pretreatment with EELT when compared with the MC group. Behavioral results showed that MC elicited significant reduction in transitions, rearings, forelimb grip strength, and latency of geotaxis. Histologically, MC induced alterations in the microanatomy of cerebral cortex, dentate gyrus, cornu ammonis 3, and cerebellum of rats. Treatment with EELT prior to MC administration significantly reduced the effect of MC on the hematological, behavioral, and ameliorated histological alterations of the brain. These findings may be attributed partially to the antioxidant property of EELT, which demonstrated protective effects against MC-induced behavioral parameters and alteration of microanatomy of rats' cerebral cortex, hippocampus, and cerebellum. In conclusion, EELT may be a valuable agent for further investigation in the prevention of acute neuropathy caused by inorganic mercury intoxication.

Effect of morin-5′-sulfonic acid sodium salt on the expression of apoptosis related proteins caspase 3, Bax and Bcl 2 due to the mercury induced oxidative stress in albino rats

Many environmental contaminants have been reported to disturb the pro-oxidant or antioxidant balance of the cells by inducing oxidative stress. Oxidative stress mediated by the HgCl2 induces DNA, protein and lipid oxidation resulted in necrosis or apoptosis, or both. Currently flavonoids are being emerging topic and reported to have antiviral, anti-inflammatory, anti- tumor and antioxidant activities. Morin is one of the flavonoid protects the cells from oxygen free radical damage and scavenges the free radicals and metals and also heals the injured cells commercially. Morin hydrate is sparingly soluble in water. Hence, the water soluble morin -5′- sulfonic acid sodium salt (NaMSA) was selected and synthesized. Aim of the present study was to analyze the effect of morin-5′-sulfonic acid sodium salt on the expression of apoptosis related proteins caspase 3, Bax and Bcl 2 due to the mercury induced oxidative stress in albino rats.. The experimental rats were exposed to sub lethal concentration of mercuric chloride (1.25mg/kg) and the ameliorating effect of NaMSA was studied by using apoptotic protein markers Bax and caspase-3 and Bcl-2. The obtained results were analyzed using one way analysis of variance by the Duncan’s Multiple comparison test to determine the level of significance (p) and p<0.05 was considered as statistically significant. Administration of mercuric chloride (1.25mg/kg) in the experimental rats increased the expression of Bax and caspase-3 and a decreased expression was noted in the Bcl-2 level compared with control bands significantly (p<0.05). On the other hand NaMSA (50mg/kg) and HgCl2 (1.25mg/kg) simultaneous administration did not bring any change in the protein expression of Bax, Caspase-3 and Bcl-2 levels compared with control rats. Hence, the membrane damage was protected, stopped the cell death and apoptosis. This could be due to the morin-5′-sulfonic acid sodium salt effective chelation action on the HgCl2 generated free radicals.

Protective effects of curcumin against mercury-induced hepatic injuries in rats, involvement of oxidative stress antagonism, and Nrf2-ARE pathway activation

Mercury (Hg) represents a ubiquitous environmental heavy metal that could lead to severe toxic effects in a variety of organs usually at a low level. The present study focused on the liver oxidative stress, one of the most important roles playing in Hg hepatotoxicity, by evaluation of different concentrations of mercuric chloride (HgCl2) administration. Moreover, the protective potential of curcumin against Hg hepatotoxic effects was also investigated. Eighty-four rats were randomly divided into six groups for a three-days experiment: control, dimethyl sulfoxide control, HgCl2 treatment (0.6, 1.2, and 2.4 mg kg-1 day-1), and curcumin pretreatment (100 mg kg-1 day-1) groups. Exposure of HgCl2 resulted in acute dose-dependent hepatotoxic effects. Administration of 2.4 mg kg-1 HgCl2 significantly elevated total Hg, nonprotein sulfhydryl, reactive oxygen species formation, malondialdehyde, apoptosis levels, serum lactate dehydrogenase, and alanine transaminase activities, with an impairment of superoxide dismutase and glutathione peroxidase in the liver. Moreover, HgCl2 treatment activated nuclear factor-E2-related factor 2-antioxidant response element (Nrf2-ARE) signaling pathway in further investigation, with a significant upregulation of Nrf2, heme oxygenase-1, and γ-glutamylcysteine synthetase heavy subunit expression, relative to control. Pretreatment with curcumin obviously prevented HgCl2-induced liver oxidative stress, which may be due to its free radical scavenging or Nrf2-ARE pathway-inducing properties. Taking together these data suggest that curcumin counteracts HgCl2 hepatotoxicity through antagonizing liver oxidative stress.

English

Aim: The present study was aimed at evaluating the effect of ascorbic acid on mercury-induced changes on the cerebellar cortex of adult Wistar rats. Methods: Thirty adult Wistar rats of average weight of 200g were randomly divided into 6 groups of 5 rats each. The animals in Group 1 (control) were administered with distilled water, Groups 2 and 3 were administered with 52mg/kg and 26.25mg/kg body weight of HgCl2 respectively while Groups 4 and 5 were administered with 52mg/kg of HgCl2 and 5mg/kg of ascorbic acid and 26.25gm/kg of HgCl2 and 5mg/kg of ascorbic acid respectively, while Group 6 was administered with 5mg/kg of ascorbic acid. The administration was through the oral route, daily for 3 weeks and the animals were humanely sacrificed. Thereafter, blood and tissue samples were harvested for analysis. Results: The result of the biochemical parameters showed a significant increase (P&lt;0.05) in the mean SOD and LPO values after the administration of mercuric chloride and ascorbic acid. Histological observation of the cerebellar cortex showed normal histo-morphology in Groups 1 and 6 while, the cerebellum in Groups 2, 3, 4 and 5 showed some degenerative, necrotic and cellular changes. Conclusion: Ascorbic acid administration has shown to ameliorate the induced degenerative changes in the cerebellum caused by mercuric chloride toxicity in Wistar rats. &nbsp; Key words: Mercuric chloride, Cerebellar cortex, Ascorbic acid, Wistar rats

Protective role of Curcuma longa extract and curcumin on mercuric chloride-induced nephrotoxicity in rats: evidence by histological architecture

Mercury (Hg) is a potent nephrotoxin. The aim of this study was to investigate the protective role of Curcuma longa extract and curcumin against HgCl2-induced nephrotoxicity. Male Sprague Dawley rats were administered HgCl2 (12 μmol kg−1, ip; once only) followed by treatment of Curcuma longa extract (200 mg kg−1, po) and curcumin (80 mg kg−1, po) for three days after 24 h of HgCl2 administration. The present results showed that mercuric chloride administration caused an impairment of renal function system which was evident from significant increase in urea, creatinine, uric acid, and blood urea nitrogen concentration in serum. In addition, the swelling in glomerulus and degenerated renal tubules with obstructed lumen was also observed by acute mercuric chloride administration. Treatment with Curcuma longa extract and curcumin was effective in restoring all variables of kidney functions near to control group, which was consistent with kidney histoarchitecture. In conclusion, these results suggest that Curcuma longa extract and curcumin protect against HgCl2-induced nephrotoxicity. This study could be important for the further understanding of mercury toxicity in renal tissues and in the development of better treatments for people and/or animals exposed to the metal.

EFFECT OF VIRGIN OLIVE OIL (&lt;i&gt;OLEA EUROPEA&lt;/i&gt;. L) ON KIDNEY FUNCTION IMPAIRMENT AND OXIDATIVE STRESS INDUCED BY MERCURIC CHLORIDE IN RATS

The study was designed to investigate the possible protective role of virgin olive oil in mercuric chloride induced renal stress, by using biochemical approaches. The effects of virgin olive oil on mercuric chloride induced oxidative and renal stress were evaluated by serum creatinine, urea and uric acid levels, kidney tissue lipid peroxidation, GSH levels, GSH-Px and GST activities. Administration of mercuric chloride induced significant increase in serum: interleukine1, interleukine6 and Tumor Necrosis Factor α (TNFα) levels, creatinine, urea and uric acid concentration showing renal stress. Mercuric chloride also induced oxidative stress, as indicate by decreased kidney tissue of GSH level, GSH-Px and GST activities along with increase the level of lipid peroxidation. Furthermore, treatment with mercuric chloride caused a marked elevation of kidney weight and decreased body weight. Virgin olive oil treatment markedly reduced elevated serum: IL1, IL6, TNFα, creatinine, urea and uric acid levels and conteracted the deterious effects of mercuric chloride on oxidative stress markers changes caused by HgCl2 in kidney. Our results indicate that virgin olive oil could have a beneficial role against mercuric chloride induced oxidative and renal stress in rat.

In vitro toxicity of mercuric chloride on rabbit spermatozoa motility and cell membrane integrity

In this in vitro study the effects of mercuric chloride on the motility and structural integrity of rabbit spermatozoa were investigated. The spermatozoa motility was evaluated using CASA method and Annexin analysis was used for detection of structural changes. The concentration of mercury in the medium varied from 5.0 to 83.3 μ g HgCl2/mL. At Time 0 the highest motility was detected in the control group (67.09 ± 8.72%). Motility in groups with mercury administration was lower in comparison with control. Significant differences were detected in groups with 50.0–83.3 μ g HgCl2/mL (P < 0.001) at Time 0. After 60 and 120 minutes of incubation with mercuric chloride the motility significantly decreased almost in all experimental groups. Progressive motility had a decreasing trend in all experimental groups. At time 60 and 120 significant differences were noted in the group receiving 6.25–83.3 μ g HgCl2/mL. Significant differences were detected in all experimental groups, except the group with the lowest mercuric chloride administration. The concentration-dependent decrease of spermatozoa progressive motility up to 50% of control was detected for groups receiving 50.0 – 83.3 μ g HgCl2/mL at Time 0, for groups receiving 12.5–83.3 μ g HgCl2/mL at Time 60 and 120, decreasing from 36.46 ± 18.73% to 1.03 ± 2.50%. Detailed evaluation of spermatozoa distance (DAP, DCL, and DSL) and velocity (VAP, VCL, and VSL) parameters as well as straightness (STR), linearity (LIN), wobble (WOB), amplitude of lateral head displacement (ALH) and beat cross frequency (BCF) of spermatozoa revealed decrease in groups with the highest mercury concentration in comparison with the control group at all time periods. Detection of spermatozoa with disordered membrane was carried out for groups with higher mercury concentrations and control, using Annexin analysis. Analysis showed higher occurrence of positive spermatozoa in the mercury exposed groups. Some Annexin positive reactions from all spermatozoa were detected in the control group. In mercury-exposed groups positive reaction proved alteration in anterial part of head (acrosome), connection part (connection piece) and in mitochondrial segment. Detected data evidently confirm adverse effects of high mercuric chloride concentrations in rabbit semen on spermatozoa motility parameters.

Renal Toxicity of Mercuric Chloride at Different Time Intervals in Rats

This study was undertaken to study the renal toxicity of mercuric chloride in rats at different periods of time. The following groups of rats were studied: i) control, ii) placebo, iii) rats injected with a single ip dose of 100 mg/kg body weight of 2, 3 dimercapto-1-propanesulfonic acid, iv) rats injected with a single ip dose of 100 mg/kg body weight of 2, 3 dimercapto-1-propanesulfonic acid (DMPS) followed by a single dose ip of 2.0 mg HgCl2/kg body weight one hour after DMPS injection v) rats injected with a single ip dose of 2.0 mg HgCl2/kg body weight. Results indicate that mercuric chloride was more toxic after 48 hours of its administration when compared to 24 hours. Mercuric chloride administration caused an impairment of renal function which was evident from a significant decrease in urine volume, urinary excretion of urea, creatinine and glomerular filteration rate (P &lt; 0.001) when compared to other treated groups. There was an increased excretion of protein, albumin and γ–-glutamyltransferase in the urine of mercuric chloride treated rats. Administration of 2, 3 dimercapto-1-propanesulfonic acid before mercuric chloride treatment caused the altered indices to return to near normal levels.

NFATc1 Identifies a Population of Proximal Tubule Cell Progenitors

Recovery from acute kidney injury requires regeneration of tubule cells. Because calcineurin induces nuclear transport of NFATc proteins, whose expression pattern correlates with the nephron segments injured by calcineurin inhibitors, we hypothesized that NFATc1 plays a role in modifying epithelial regeneration after injury. To test this, we induced proximal tubular cell (PTC) injury in Balb/c mice and Nfatc1(+/-) mice with mercuric chloride; the PTCs of Nfatc1(+/-) mice demonstrated increased apoptosis, sustained injury, and delayed regeneration. To attenuate NFATc1 activity further, we injected cyclosporin A daily. Cyclosporin A-treated Nfatc1(+/-) mice demonstrated rapid and severe injury after administration of mercuric chloride, with increased serum creatinine, increased apoptosis, decreased PTC proliferation, and increased mortality compared with similarly treated wild-type mice. Using a novel NFATc1 transgenic line that reports activation of an NFATc1 enhancer domain critical for NFATc1 autoamplification, we demonstrated accentuated NFATc1 expression in a PTC subpopulation after mercuric chloride-induced injury. In addition, NFATc1-labeled, apoptosis-resistant PTCs proliferated to repair the damaged proximal tubule segment. These data provide evidence for a resident progenitor PTC population and suggest a role for NFATc1 in the regeneration of injured proximal tubules.

Influence of Dietary Protein Levels on the Fate of Inorganic Mercury in Mice

Influence of dietary protein levels on mercury (Hg) fate and on tissue metallothionein (MT) levels was investigated in mice. Twenty-four hr after single administration of mercuric chloride (2.5 mg Hg/kg, subcutaneous), the hepatic Hg concentration was enhanced by dietary protein deficiency, whereas the levels in other tissues and excrements were not affected. At that time, MT inductions by mercuric chloride in liver and kidney were suppressed by dietary protein deficiency, despite no observable differences in basal levels. Thus, Hg levels in the liver and kidney showed little correlation with MT levels. A further experiment demonstrated an enhancement of Hg concentration in the liver by dietary protein deficiency at 3 and 12hr but not at 1hr, and the Hg concentration in the kidney was transiently enhanced at 3 hr. Accordingly, the differences in Hg fate would arise considerably earlier, probably before MT induction. The present results suggest that dietary protein status modifies the fate of inorganic Hg, especially in the liver, probably independent of the differences in dietary protein level-dependent varying levels of MT.

Evaluation of protective efficacy of Spirulina fusiformis against mercury induced nephrotoxicity in Swiss albino mice

The toxicity of mercury to animals and man is well established and this depends greatly on the form of the mercury compounds. In most animals’ species, including man, the kidney is the main site of deposition of inorganic mercury and target organ for its toxicity. In the present study Spirulina fusiformis (a cyanobacterium, belongs to family – Oscillatoriaceae) has been investigated as a possible modifier of mercury induced renal damages in Swiss albino mice. Animals were divided into four groups. (i) Control group – only vehicle (0.9% NaCl) was administered as i.p. (ii) HgCl 2 treated group – 5.0 mg/kg b.wt. HgCl 2 was administered as i.p. (iii) Spirulina treated group – 800 mg/kg b.wt. Spirulina extract was administered orally. (iv) Combination group – S. fusiformis was administered 10 days before mercuric chloride administration and continued upto 30 days after mercuric chloride administration (5.0 mg/kg b.wt.). The animals were autopsied on 1, 3, 7, 15 and 30 days after treatment and the activity of alkaline phosphatase (ALP), acid phosphatase (ACP), lactate dehydrogenase (LDH) and MDA (malondialdehyde) level were measured in kidney homogenates. The results indicated that there was a time-dependent significant enhancement in MDA content and ACP activity and decrease in LDH and ALP activity observed after HgCl 2 treatment. Mercury intoxication also induces pathological alterations in the kidney such as degeneration of glomerulus, proximal and distal tubules. A dose-dependent mortality was also observed following administration of different doses of HgCl 2. In combined treatment of Spirulina with HgCl 2, a significant decrease in MDA content and ACP activity and elevation in LDH and ALP activity was observed as compared to HgCl 2 treated group. Spirulina pre- and post-treatment with mercury also significantly reduces pathological alterations in kidney. Thus, the results from the present study suggest that S. fusiformis can significantly modify the renal damages against mercuric chloride induced toxicity.

Protective effect of Kundur (Boswellia serrata) against mercuric chloride induced nephrotoxicity in rats

The effect of Kundur (oleo-gum resin of Boswellia serrata) and its fractions viz: methanol soluble (MS) and methanol insoluble (MI) were investigated on mercuric chloride induced nephrotoxicity in rats. The animals of group I and II were administered with 1% carboxymethyl cellulose (CMC) (1,000 mg/kg, p.o.) and the animals of groups III, IV and V were administered with Kundur (1,000 mg/kg, p.o.), MS (650 mg/kg, p.o.) and MI (350 mg/kg, p.o.) respectively for ten days. On 10th day a single dose of the mercuric chloride (3 mg/kg, 5.c.) was also administered to all groups except the group I which received only 1% CMC (10 ml/kg, p.o.). After two days of mercuric chloride administration the blood samples of each animal were collected and analyzed for blood urea nitrogen and creatinine concentration. Rats fed with Kundur and MI fraction showed a significant prevention in the rise of serum markers while MS failed to prevent the rise of these serum makers. These results suggest that Kundur and MI fraction may have potential to reduce the nephrotoxicity in rats.

Modification of mercury-induced biochemical alterations in blood of Swiss albino mice by Spirulina fusiformis

The present investigation has been undertaken to evaluate the role of Spirulina fusiformis in modifying the mercury-induced biochemical alterations in Swiss albino mice. Animals were divided into four groups: (i) control group – only vehicle (0.9% NaCl/olive oil) was given; (ii) HgCl 2 treated group – 5.0 mg/kg b.w. HgCl 2 administered as i.p.; (iii) Spirulina treated group – 800 mg/kg b.w. Spirulina extract was administered orally; (iv) combination group – S. fusiformis was administered 10 days before mercuric chloride administration and continued up to 30 days after mercuric chloride administration (5.0 mg/kg b.w.). The animals were sacrificed on 1, 3, 7, 15 and 30 days and the activity of serum alkaline and acid phosphatase, serum iron level, serum calcium level, blood lipid peroxidation content and blood glutathione (GSH) level were measured. In the present investigation, mercury intoxication causes significant increase ( P < 0.001) in calcium level, acid phosphatase and lipid peroxidation content and significant decrease in iron level, alkaline phosphatase and glutathione level. Spirulina pre- and post-treatment with mercury prevented or reduces mercury-induced alterations in terms of calcium level, iron level, acid and alkaline phosphatase activity in serum, and lipid peroxidation and GSH level in blood. Thus from the present investigation, it can be concluded that Spirulina pre- and post-treatment with HgCl 2 significantly modulate or modify mercury-induced biochemical alteration in blood of Swiss albino mice.