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1.
The toxicity of heavy metals such as mercury (Hg) in humans and animals is well documented. The kidney is the primary deposition site of inorganic-Hg and target organ of its toxicity. The present study investigated the protective efficacy of flaxseed lignan-Secoisolariciresinol diglucoside (SDG) on nephrotoxicity induced by mercuric chloride (HgCl2). Rats were intraperitoneally injected with HgCl2 (2 mg/kg/day) and renal toxicity was induced. Subcutaneous administration of rats with SDG (5 mg/kg/day) as a pre-treatment caused a significant reversal of HgCl2 induced increase in blood urea, creatinine, glutathione s-transferase and catalase (CAT). On the other hand, administration of SDG with HgCl2 restored normal levels of albumin and superoxide dismutase (SOD). Histological examination of kidneys confirmed that pre-treatment of SDG before HgCl2 administration significantly reduced its pathological effects. Thus, the results of the present investigation suggest that SDG can significantly reduce renal damage, serum and tissue biochemical profiles caused by HgCl2 induced nephrotoxicity. Hence, SDG may be recommended for clinical trials in the treatment of kidney disorders caused by exposure to Hg. 相似文献
2.
The present study was designed to investigate the effect of mercuric chloride administration on copper, zinc, and iron concentrations in the liver, kidney, lung, heart, spleen, and muscle of rats. The results showed that after dose and time exposure to mercuric chloride, the concentration of mercury in the six tissues was significantly elevated. Data showed that there were no interaction between mercury and tissue iron. There was a considerable elevation of the content of copper in the kidney and liver. The most significant changes in the copper concentration took place in the kidneys. About a twofold increase in the copper content of the kidney was noted after exposure to mercuric chloride (3 mg and 5 mg/kg). Only slight elevations in the copper content occurred in the liver, especially in high dose and longer exposure time. In the remaining organs, the copper content was not changed significantly ( p>0.05). The most significant changes in the zinc concentration took place in liver, kidney, lung, and heart (5 mg/kg). Marked changes in kidney zinc concentrations were observed at any of the specified doses. Zinc concentrations were significantly increased in kidney of rats sacrificed 9–48 h after sc injection of HgCl 2 (5 mg/kg); in liver obtained from rats at 18, 24, or 48 h after injection; and in lung after 24 or 48 h of treatment. The heart and spleen zinc concentrations were elevated at 24 and 48 h after injection of HgCl 2 (5 mg/kg), respectively. The results of this study implicate that effects on copper and zinc concentrations of the target tissues of mercury may play an important role in the pathogenesis of acute mercuric chloride intoxication. 相似文献
3.
Many glomerular diseases are associated with changes in the expression and distribution in the components of extracellular matrix. A remarkable feature in acute renal failure induced by mercuric chloride in rats was large fibronectin (Fn) deposits in kidneys 1 h post-HgCl 2 injection (5 mg/kg body wt., s.c.). Our study examined some mechanisms as potential explanation of the early Fn deposits in mercuric chloride induced acute renal failure. Total tissue mRNA of livers and kidneys of control and treated rats were used in Northern blot to determine whether accumulation of Fn in kidney is associated with increases in the expression of this protein in the kidney and/or in the liver. Analysis of Fn levels by Western blot were also performed. Northern blot did not show significant difference between control and treated rats, while the abundance of polymerized-Fn in kidney tissue was increased 1 h and 5 h post HgCl 2 injection.HgCl 2 influence on Fn folding was studied in vitro to detect possible conformational changes that could altered its normal pattern of matrix assembly and/or binding to different ligands. In this context HgCl 2 binding to Fn was measured following native thryptophan fluorescence of Fn in the presence of HgCl 2 (0.5–250 mM). Binding parameters for the HgCl 2–Fn complex formation were Kd = (1.6 ± 0.2) 10 –4 M; n = 1 ± 0.3, indicating a low apparent affinity and one type binding site. Thermal denaturation of Fn showed, between 30–60°C, a soft reversible conformational change, while between 75–80°C a highly and irreversible transition is produced suggesting a modification of the tertiary structure. HgCl 2 abolished this transition. The kinetic of thermal unfolding of Fn was also measured and the effects observed due to HgCl 2 presence reinforced the previous data. Finally, the effect of HgCl 2 on Fn binding to denatured collagen (gelatin) was also measured as an index of the effect of this cation on biological properties of Fn. Fn binds gelatin strongest in the presence of HgCl 2.Our results suggest that higher Fn deposits in kidney treated rats seems not to be associated to augmented mRNA-Fn neither in kidney nor in liver. On the other hand, increased levels of polymerized Fn abundance was observed in kidney tissue from mercury-treated rats. We also describe that HgCl 2 promotes, in vitro, conformational changes on Fn structure, inducing its denaturation and increasing its binding to gelatin, all events that could be related to the Fn deposits in renal tissues of HgCl 2-treated rats, and could be expected in other situations that promoted interstitial fibrosis, not associated to overexpression of matrix-proteins. 相似文献
4.
This work investigated the preventive effect of diphenyl diselenide [(PhSe) 2] on renal and hepatic toxicity biomarkers and oxidative parameters in adult mice exposed to mercury chloride (HgCl 2). Selenium (Se) and mercury (Hg) determination was also carried out. Mice received a daily oral dose of (PhSe) 2 (5.0 mg/kg/day) or canola oil for five consecutive days. During the following five days, the animals were treated with a daily subcutaneous dose of HgCl 2 (5.0 mg/kg/day) or saline (0.9%). Twenty-four hours after the last HgCl 2 administration, the animals were sacrificed and biological material was obtained. Concerning toxicity biomarkers, Hg exposure inhibited blood δ-aminolevulinic acid dehydratase (δ-ALA-D), serum alanine aminotransferase (ALT) activity and also increased serum creatinine levels. (PhSe) 2 partially prevented blood δ-ALA-D inhibition and totally prevented the serum creatinine increase. Regarding the oxidative parameters, Hg decreased kidney TBARS levels and increased kidney non-protein thiol levels, while (PhSe) 2 pre-treatment partially protected the kidney thiol levels increase. Animals exposed to HgCl 2 presented Hg content accumulation in blood, kidney and liver. The (PhSe) 2 pre-treatment increased Hg accumulation in kidney and decreased in blood. These results show that (PhSe) 2 can be efficient in protecting against these toxic effects presented by this Hg exposure model. 相似文献
5.
This study evaluated the effects of HgCl 2 on renal parameters in nonlactating and lactating rats and their pups, as well as the preventive role of ZnCl 2. Rats received 27 mg kg ?1 ZnCl 2 for five consecutive days and 5 mg kg ?1 HgCl 2 for five subsequent days (s.c.). A decrease in δ‐aminolevulinic acid dehydratase ( δ‐ALA‐D) activity in the blood and an increase in urine protein content in renal weight as well as in blood and urine Hg levels were observed in lactating and nonlactating rats from Sal―Hg and Zn―Hg groups. ZnCl 2 prevented partially the δ‐ALA‐D inhibition and the proteinuria in nonlactating rats. Renal Hg levels were increased in all HgCl 2 groups, and the ZnCl 2 exposure potentiated this effect in lactating rats. Nonlactating rats exposed to HgCl 2 exhibited an increase in plasma urea and creatinine levels, δ‐ALA‐D activity inhibition and histopathological alterations (necrosis, atrophic tubules and collagen deposition) in the kidneys. ZnCl 2 exposure prevented the biochemical alterations. Hg‐exposed pups showed lower body and renal weight and an increase in the renal Hg levels. In conclusion, mercury‐induced nephrotoxicity differs considerably between lactating and nonlactating rats. Moreover, prior exposure with ZnCl 2 may provide protection to individuals who get exposed to mercury occupationally or accidentally. Copyright © 2014 John Wiley & Sons, Ltd. 相似文献
6.
It is well known that antioxidants containing sulfhydryl (−SH) groups are protective against the toxic effects of mercury.
The current study was designed to elucidate the mechanism(s) of the cytoprotective effects of glutathione (GSH) and N-acetylcysteine (NAC) against the toxicity of inorganic mercury (HgCl 2) in neuroblastoma cells (N-2A). The obtained results demonstrated the protective effects of these compounds in a dose dependant
manner up to 95 and 74% cell viability, respectively as compared to the control of HgCl 2 of 10%. The administration of buthionine sulfoximine (BSO), an inhibitor of GSH synthesis, increased the toxicity of HgCl 2 in a dose dependent manner. Moreover, BSO treatment attenuated the levels of the cellular free −SH concentrations at low
concentrations (1–100 μM) of HgCl 2. The data also show that cellular thiol concentrations were augmented in the presence of GSH and NAC and these compounds
were cytoprotective against HgCl 2 and this is due to up regulating of GSH synthesis. A reduction in intracellular levels of GSH was observed with treatment
of HgCl 2. In addition, the ratio of GSH/GSSG increased from 16:1 to 50:1 from 1 to 10 μM concentration of HgCl 2. The ratio of GSH/GSSG then decreased from 4:1 to 0.5:1 with the increase of concentration of HgCl 2 between 100 μM and 1 mM due to the collapse of the N-2A cells. It was of interest to note that the synthesis of GSH was stimulated
in cells exposed to low concentration of HgCl 2 when extra GSH is available. These data support the idea that the loss of GSH plays a contributing role to the toxic effects
of HgCl 2 and that inorganic mercury adversely affects viability, through altering intracellular −SH concentrations. The data further
indicate that the availability of GSH to the cells may not be sufficient to provide protection against mercury toxicity and
the de novo synthesis of intracellular GSH is required to prevent the damaging effects of mercury. 相似文献
7.
Our objective was to study if the phycobiliproteins of the cyanobacterium Pseudanabanea tenuis rich in phycoerythrin protect renal cells against mercury-caused oxidative stress and cellular damage in the kidney. We used
40 male mice that were assigned into five groups: a control group that received phosphate buffer (PB) and saline and four
treatment groups which received either PB+HgCl 2, PB+phycobiliproteins, or HgCl 2+phycobiliproteins. The kidneys of the mice were used to determine lipid peroxidation and quantification of reactive oxygen
species, oxidized glutathione, and peroxidase activities (catalase and glutathione peroxidase) and were also examined histologically.
Our results demonstrated that HgCl 2 causes oxidative stress and cellular damage and that all doses of phycobiliproteins prevented the increase of oxidative markers
and partially protected against HgCl 2-caused cell damage. This is the first report which applied phycobiliproteins of P. tenuis rich in c-phycoerythrin, like antioxidants against mercury chloride-caused oxidative stress and renal damage. 相似文献
8.
Right ventricle systolic dysfunction is a major risk factor for death and heart failure after myocardial infarction (MI). Heavy metal exposure has been associated with the development of several cardiovascular diseases, such as MI. The aim of this study was to investigate whether chronic exposure to low doses of mercury chloride (HgCl 2) enhances the functional deterioration of right ventricle strips after MI. Male Wistar rats were divided into four groups: Control (vehicle); HgCl 2 (exposure during 4 weeks- 1st dose 4.6 µg/kg, subsequent dose 0.07 µg/kg/day, i.m. to cover daily loss); MI surgery induced and HgCl 2-MI groups. One week after MI, the morphological and hemodynamic measurements and isometric tension of right ventricle strips were investigated. The chronic HgCl 2 exposure did not worsen the injury compared with MI alone in the morphological or hemodynamic parameters evaluated. At basal conditions, despite similar maximum isometric force at L-max, relaxation time was increased in the MI group but unaffected in the HgCl 2-MI compared to the Control group. Impairment of the sarcoplasmic reticulum (SR) function and reduction in the sarcolemmal calcium influx were observed in MI group associated with SERCA2a reduction and increased PLB protein expression. Induction of MI in chronic HgCl 2 exposed rats did not cause any alteration in the developed force at L-max, lusitropic function or −dF/dt except for a tendency of a reduction SR function. These findings could be partially explained by the normalization in the sarcolemmal calcium influx and the increase in NCX protein expression observed only in this group. These results suggest that chronic exposure to low doses of HgCl 2 prevents the impaired SR function and the reduced sarcolemmal calcium influx observed in MI likely by acting on NCX, PLB and SERCA2a protein expression. 相似文献
9.
The effectiveness of 2,3-dimercaptopropanol (BAL) and meso-2,3-dimercaptosuccinic acid (DMSA) on HgCl 2-induced nephrotoxicity was studied in the rat. Seven groups of adult male rats were given a single sc toxic dose of HgCl 2 (0.68 mg/kg) followed by 0.9% saline (positive control group), BAL (15, 30, and 60 mg/kg) or DMSA (50, 100, and 200 mg/kg)
administered ip at 0, 24, 48, and 72 h thereafter. Although the renal function of HgCl 2-exposed rats was slightly improved after BAL administration, Hg concentrations in the kidney were only reduced at 60 mg/kg.
In addition, the protective effect of BAL was not dose-related. In contrast to BAL, DMSA was effective in increasing the urinary
excretion of Hg and in reducing the renal Hg content. These results show that DMSA would be more effective than BAL in preventing
or in protecting against inorganic Hg-induced nephrotoxicity. 相似文献
10.
Mercury is a toxic and bio-accumulative heavy metal of global concern. While good deals of research have been conducted on the toxic effects of mercury, little is known about the mechanisms involved in the pathogenesis of male reproductive dysfunction induced by mercury. Therefore, the purpose of this study was to assess the effects and underlying mechanisms of chronic mercury exposure at low levels on male reproductive system of rats. Three-month-old male Wistar rats were divided into two groups and treated for 60 days with saline (i.m., Control) and HgCl 2 (i.m. 1 st dose: 4.6 µg/kg, subsequent doses 0.07 µg/kg/day). We analyzed sperm parameters, hormonal levels and biomarkers of oxidative stress in testis, epididymis, prostate and vas deferens. Mercury treatment decreased daily sperm production, count and motility and increased head and tail morphologic abnormalities. Moreover, mercury treatment decreased luteinizing hormone levels, increased lipid peroxidation on testis and decreased antioxidant enzymes activities (superoxide dismutase and catalase) on reproductive organs. Our data demonstrate that 60-day chronic exposure to low concentrations of HgCl 2 impairs sperm quality and promotes hormonal imbalance. The raised oxidative stress seems to be a potential mechanism involved on male reproductive toxicity by mercury. 相似文献
11.
Alveolar macrophages collected by pulmonary lavage from male Fisher-344 rats at intervals (24–72 h) after HgCl 2 injection (1–5 mg/kg, sc) were analyzed by several techniques. Within 24–72 h, the macrophages showed morphological signs
of activation (hypertrophy and ruffled plasma membrane). Lipid peroxidation (increased malondialdehyde concentration) was
not detected until 48 h. Dose- and time-related effects of HgCl 2 on malondialdehyde concentration and time-related effects of HgCl 2 on malondialdehyde concentration and mercury content of alveolar macrophages were observed 24–72 h postinjection. Diminished
cell viability occurred only at 72 h after the highest dosage of HgCl 2. This study demonstrates that the alveolar macrophage was a cellular target for mercury toxicity following parenteral exposure
to HgCl 2. 相似文献
12.
Zebrafish ( Danio rerio) has been adopted as a model for behavioral, immunological and toxicological studies. Mercury is a toxic heavy metal released into the environment. There is evidence indicating that heavy metals can modulate ionotropic receptors, including the purinergic receptor P2X7. Therefore, this study evaluated the in vivo effects of acute exposure to mercury chloride (HgCl 2) in zebrafish larvae and to investigate the involvement of P2X7R in mercury-related toxicity. Larvae survival was evaluated for 24 h after exposure to HgCl 2, ATP or A740003. The combination of ATP (1 mM) and HgCl 2 (20 μg/L) decreased survival when compared to ATP 1 mM. The antagonist A740003 (300 and 500 nM) increased the survival time, and reversed the mortality caused by ATP and HgCl 2 in association. Quantitative real time PCR showed a decrease of P2X7R expression in the larvae treated with HgCl 2 (20 μg/L). Evaluating the oxidative stress our results showed decreased CAT (catalase) activity and increased MDA (malondialdehyde) levels. Of note, the combination of ATP with HgCl 2 showed an additive effect. This study provides novel evidence on the possible mechanisms underlying the toxicity induced by mercury, indicating that it is able to modulate P2X7R in zebrafish larvae. 相似文献
13.
Ten Escherichia coli strains isolated from five different aquatic environments representing three distinct geographical regions of India showed significantly high levels of tolerance to the inorganic form of mercury, i.e., mercuric chloride (HgCl 2). MRD14 isolated from the Dal Lake (Kashmir) could tolerate the highest concentration of HgCl 2, i.e., 55 g/mL, and MRF1 from the flood water of the Yamuna River (Delhi) tolerated the lowest concentration, i.e., 25 g/mL. All ten strains revealed the presence of a plasmid of approximately 24 kb, and transformation of the isolated plasmids into the mercury-sensitive competent cells of E. coli DH5 rendered the transformants resistant to the same concentration of mercury as the wild-type strains. Mating experiments were performed to assess the self-transmissible nature of these promiscuous plasmids. The transfer of mercury resistance from these wild-type strains to the mercury-sensitive, naladixic acid-resistant E. coli K12 (F –lac+) strain used as a recipient was observed in six of the nine strains tested. Transconjugants revealed the presence of a plasmid of approximately 24 kb. An evaluation of the mechanism of mercury resistance in the three most efficient strains (MRG12, MRD11, and MRD14) encountered in our study was determined by cold vapor atomic absorption spectroscopy (CV-AAS), and it was noted that resistance to HgCl 2 was conferred by conversion of the toxic ionic form of mercury (Hg ++) to the nontoxic elemental form (Hg 0) in all three strains. MRD14 volatilized mercury most efficiently. 相似文献
14.
This work investigated zinc (Zn) and mercury (Hg) effects on oxidative parameters, markers of toxicity and metal levels in different tissues from non-lactating rats (NLR) and lactating rats (LR). Adult NLR and LR received ZnCl 2 (27 mg/kg) or saline (0.9%) subcutaneously and after 24 h they received HgCl 2 (5 mg/kg) or saline (0.9%). Twenty four hours later, they were sacrificed and the preparation of biological material and biochemical analyses were performed. With respect to oxidative parameters, Hg exposure decreased kidney total SH levels from NLR and LR and hepatic catalase activity (not statistically significant) in NLR. Zinc pre-treatment partly prevented the decrease of kidney total SH levels in LR. Zinc per se increased hepatic non-protein SH levels of NLR and LR. Regarding toxicity markers, Hg exposure inhibited the δ-aminolevulinic acid dehydratase (δ-ALA-D) activity from kidney and liver of NLR, inhibited serum alanine aminotransferase (ALT) activity of LR and increased serum creatinine and urea levels of NLR and LR. Zinc pre-exposure prevented the enzymatic alterations caused by Hg. NLR and LR Hg exposed presented accumulation of mercury in the kidney, liver, blood and urine. Zinc pre-treatment prevented this accumulation partly in NLR liver and blood and completely in LR kidney and liver. These results show that NLR and LR are differently sensitive to HgCl 2 and that ZnCl 2 showed a promising effect against Hg toxicity. 相似文献
15.
Mercuric chloride (HgCl 2) is a highly toxic compound, which can cause nephrotoxic damage. In the present study effects of HgCl 2 on mitochondria integrity and energy metabolism, as well as antidotal effects of 2,3-dimercaptopropane-1-sulfonate (DMPS)
were investigated in the opossum kidney derived cell line (OK). OK cell monolayers were incubated during 0, 1, 3, 6, and 9
h in serum-free culture medium containing 15 μM HgCl 2, either in the absence or in the presence of 60 μM DMPS in a 1:4 ratio. Intracellular ATP content, MTT reduction, and HSP70/HSP90 induction were studied; confocal, transmission
electron microscopy, and light microscopy studies were also performed. For confocal analysis, a mitochondrial selective probe
(MitoTracker Red CMXH2Ros) was used. Antioxidant activity of DMPS was also studied by the scavenging of the free radical 2,
2-diphenyl-1-picrylhydrazyl (DPPH) technique. A decrease of ATP content, an impaired ability to reduce tetrazolium, and dramatic
changes on cellular and mitochondrial morphology, and energetic levels were found after either 6 or 9 h of HgCl 2 exposure. Increased expression of HSP90 and HSP70 were also seen. When OK cells were co-incubated with HgCl 2 and DMPS, cellular morphology, viability, intracellular ATP, and mitochondrial membrane potential were partially restored;
a protective effect on mitochondrial morphology was also seen. DMPS also showed potent antioxidant activity in vitro. Mitochondrial protection could be the cellular mechanism mediated by DMPS in OK cells exposed to a toxic concentration of
HgCl 2. 相似文献
16.
This study was aimed to isolate Hg-resistant bacteria from contaminated sediments of the Orbetello Lagoon in Italy and to assess their possible use as biofilms in bioremediation processes. Enrichment cultures prepared from contaminated sediments in the presence of 0.05 mM of mercury and under aerobic conditions allowed the isolation of five heterotrophic bacterial strains. 16S rDNA gene sequencing assigned the isolated strains to the genera Pseudomonas and Psychrobacter. For the first time mercury-resistant bacterial strains belonging to the genus Psychrobacter were evidenced. Minimum inhibitory concentrations in the presence of HgCl 2 and of CH 3HgCl showed high levels of resistance. EC50 values for the isolated bacterial strains in the presence of HgCl 2 and of CH 3HgCl confirmed the adaptation to the metal. Hg-resistant strains ORHg1, ORHg4 and ORHg5 showed the capacity to volatilize inorganic and organic mercury to elemental mercury, and formed biofilms on pumice particles, and were shown to play a role in the removal of mercury from sediment leachates. This study reports isolation and characterization of new Hg-resistant bacterial strains and provides novel insight into their possible use in bioremediation processes of mercury polluted sediments. 相似文献
17.
To assess effects of epidermal growth factor (EGF) and pegylated granulocyte colony‐stimulating factor (P‐GCSF; pegfilgrastim) administration on the cellular origin of renal tubular epithelium regenerating after acute kidney injury initiated by mercuric chloride (HgCl 2). Female mice were irradiated and male whole bone marrow (BM) was transplanted into them. Six weeks later recipient mice were assigned to one of eight groups: control, P‐GCSF+, EGF+, P‐GCSF+EGF+, HgCl 2, HgCl 2+P‐GCSF+, HgCl 2+EGF+ and HgCl 2+P‐GCSF+EGF+. Following HgCl 2, injection tubular injury scores increased and serum urea nitrogen levels reached uraemia after 3 days, but EGF‐treated groups were resistant to this acute kidney injury. A four‐in‐one analytical technique for identification of cellular origin, tubular phenotype, basement membrane and S‐phase status revealed that BM contributed 1% of proximal tubular epithelium in undamaged kidneys and 3% after HgCl 2 damage, with no effects of exogenous EGF or P‐GCSF. Only 0.5% proximal tubular cells were seen in S‐phase in the undamaged group kidneys; this increased to 7–8% after HgCl 2 damage and to 15% after addition of EGF. Most of the regenerating tubular epithelium originated from the indigenous pool. BM contributed up to 6.6% of the proximal tubular cells in S‐phase after HgCl 2 damage, but only to 3.3% after additional EGF. EGF administration attenuated tubular necrosis following HgCl 2 damage, and the major cause of this protective effect was division of indigenous cells, whereas BM‐derived cells were less responsive. P‐GCSF did not influence damage or regeneration. 相似文献
18.
Acute effects of mercury on mouse blood, kidneys, and liver were evaluated. Mice received a single dose of mercuric chloride
(HgCl 2, 4.6 mg/kg, subcutaneously) for three consecutive days. We investigated the possible beneficial effects of antioxidant therapy
( N-acetylcysteine (NAC) and diphenyl diselenide (PhSe) 2) compared with the sodium salt of 2,3-dimercapto-1-propanesulfonic acid (DMPS), an effective chelating agent in HgCl 2 exposure in mice. We also verified whether metallothionein (MT) induction might be involved in a possible mechanism of protection
against HgCl 2 poisoning and whether different treatments would modify MT levels and other toxicological parameters. The results demonstrated
that HgCl 2 exposure significantly inhibited δ-aminolevulinate dehydratase (δ-ALA-D) activity in liver and only DMPS treatment prevented
the inhibitory effect. Mercuric chloride caused an increase in renal non-protein thiol groups (NPSH) and none of the treatments
modified renal NPSH levels. Urea concentration was increased after HgCl 2 exposure. NAC plus (PhSe) 2 was partially effective in protecting against the effects of mercury. DMPS and (PhSe) 2 were effective in restoring the increment in urea concentration caused by mercury. Thiobarbituric acid-reactive substances
(TBARS), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) activities and ascorbic acid levels were not
modified after mercury exposure. Mercuric chloride poisoning caused an increase in hepatic and renal MT levels and antioxidant
treatments did not modify this parameter. Our data indicated a lack of therapeutic effect of the antioxidants tested. 相似文献
19.
Parenteral administration of mercuric chloride (HgCl 2) to rats enhanced lipid peroxidation in liver, kidney, lung, testis, and serum (but not in heart, spleen, or muscle), as
measured by the thiobarbituric acid reaction for malondialdehyde (MDA) in fresh tissue homogenates and body fluids. After
sc injection of HgCl 2 (5 mg/kg body wt), MDA concentrations in liver and kidney became significantly increased by 9 h and reached peak values at
24 h. Dose-response studies were carried out with male albino rats of the Fisher-344 strain (body wt 170–280 g) injected with
1, 3, 5 mg Hg/kg as HgCl 2 and sacrificed after 24 h. In time-response studies, animals were administered 5 mg Hg/kg as HgCl 2 and sacrificed after 3, 9, 18, 24, and 48 h. Studies in the authors' laboratory have shown that (1) concentrations of MDA
are increased in targets (liver, kidney, lung, and testis) of HgCl 2-treated rats; (2) severity of hepatotoxicity and nephrotoxicity is generally consistent with the elevation of Hg and MDA
concentrations, based upon the time-course and dose-effect relationships observed after administration of HgCl 2 to rats; and (3) concentrations of MDA are reduced in target tissues after pretreatment with antioxidants and chelators to
HgCl 2-treated rats. The results of this study implicate that the lipid peroxidation is one of the molecular mechanisms for cell
injury in acute HgCl 2 poisoning. 相似文献
20.
Minimal inhibitory concentration values of HgCl 2 and 5 organomercurials were determined against 24 mercury-resistant N 2-fixing soil bacteria previously isolated from soil and identified in our laboratory. These bacterial strains also displayed
multiple antibiotic resistant properties. Typical growth pattern of a highly mercury-resistant Beijerinckia sp (KDr 2) was studied in liquid broth supplemented with toxic levels of mercury compounds. Four bacterial strains were selected for
determining their ability to volatilize mercury and their Hg-volatilizing capacity was different. Cell-free extracts prepared
from overnight mercury-induced cells catalyzed Hg 2+-induced NADPH oxidation. Specific activities of Hg 2+-reductase which is capable of catalyzing conversion of Hg 2+ →Hg(o) of 10 Hg-resistant bacterial strains are also reported. 相似文献
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