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1.
In the present investigation, the effects of mercuric chloride (HgCl 2) on the neurobehavioural and neurochemical disruption in mice offspring was studied. A total of thirty pregnant mice were divided into six groups. Group II and III were received 150 and 300 ppm of curcumin respectively. Group IV was given 10 ppm of HgCl 2. Group V and VI were given 10 ppm of HgCl 2 with 150 and 300 ppm of curcumin respectively. In this study, treatment started from day one of pregnancy and continued until post-natal day 15 (PD 15). During weaning period, three pups in each experimental group were marked and were subjected to behavioral, physical and biochemical tests. The results revealed decreased body weight, delayed hair growth and eye opening. HgCl 2 treated pups taken more time in righting, rotating reflexes to return to normal placement, cliff avoidance compared to that of control group. HgCl 2 exposed pups showed memory and learning deficits. Anxiety behavior in treating pups was increased. Biochemical investigations showed decreased level of dopamine (DA), serotonin (5-HT) and acetylcholinesterase (AChE) in forebrain of treated pups compared to the control and curcumin groups. The protective effect of curcumin doses were significant compared to HgCl 2 group. The results indicated that the administration of curcumin showed effective activity towards biochemical and behavioral disorders obtained with the HgCl 2 treated animals. Overall, the curcumin administration revealed increased cognetion and anxiety behaviors in the treated animals. Conclusively, curcumin has a good benefits for health which can use to avoid toxicants such as Hg and other heavy metals. 相似文献
2.
Mercury is a toxic, environmentally heavy metal that can cause severe damage to all organs, including the nervous system. The functions of puerarin include antioxidant, anti-inflammatory, nerve cell repair, regulation of autophagy, and so forth. But because of the limited oral absorption of puerarin, it affects the protective effect on brain tissue. The nano-encapsulation of Pue can improve its limitation. Therefore, this study investigated the protective effect of Pue drug-loaded PLGA nanoparticles (Pue-PLGA-nps) on brain injury induced by mercuric chloride (HgCl 2) in mice. The mice were divided into normal saline (NS) group, HgCl 2 (4 mg/kg) group, Pue-PLGA-nps (50 mg/kg) group, HgCl 2 + Pue (4 mg/kg + 30 mg/kg) group, and HgCl 2 + Pue-PLGA-nps (4 mg/kg + 50 mg/kg) group. After 28 days of treatment, the mice were observed for behavioral changes, antioxidant capacity, autophagy and inflammatory response, and mercury levels in the brain, blood, and urine were measured. The results showed that HgCl 2 toxicity caused learning and memory dysfunction in mice, increased mercury content in brain and blood, and increased serum levels of interleukin (IL-6), IL-1β, and tumor necrosis factor-α in the mice. HgCl 2 exposure decreased the activity of T-AOC, superoxide dismutase, and glutathione peroxidase, and increased the expression of malondialdehyde in the brain of mice. Moreover, the expression levels of TRIM32, toll-like receptor 4 (TLR4), and LC3 proteins were upregulated. Both Pue and Pue-PLGA-nps interventions mitigated the changes caused by HgCl 2 exposure, and Pue-PLGA-nps further enhanced this effect. Our results suggest that Pue-PLGA-nps can ameliorate HgCl 2-induced brain injury and reduce Hg accumulation, which is associated with inhibition of oxidative stress, inflammatory response, and TLR4/TRIM32/LC3 signaling pathway. 相似文献
3.
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
4.
The hydrocarbon utilizing haloarchaea, Haloferax (two strains), Halobacterium and Halococcus from a hypersaline coastal area of the Arabian Gulf, had the potential for resistance and volatilization of Hg 2+. Individual haloarchaea resisted up to between 100 and 200 ppm HgCl 2 in hydrocarbon free media with salinities between 1 and 4 M NaCl, but only up to between 20 and 30 ppm in a mineral medium
containing 3 M NaCl, with 0.5% (w/v) crude oil, as a sole source of carbon and energy. Halococcus and Halobacterium volatilized more mercury than Haloferax. The individual haloarchaea consumed more crude oil in the presence of 3 M NaCl than in the presence of 2 M NaCl. At both
salinities, increasing the HgCl 2 concentration in the medium from 0 to 20 ppm resulted in decreasing the oil consumption values by the individual haloarchaea.
However, satisfactory oil consumption still occurred in the presence of 10 ppm HgCl 2. It was concluded that haloarchaea with the combined potential for mercury resistance and volatilization and hydrocarbon
consumption could be useful in removing toxic mercury forms effectively from oil free, mercury contaminated, hypersaline environments,
and mercury and oil, albeit less effectively, from oily hypersaline environments. 相似文献
5.
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
6.
Mercury exposure is second-most common cause of metal poisoning which is quite stable and biotransformed to highly toxic metabolites thus eliciting biochemical alterations and oxidative stress. The aim of present study describes the protective effect of selenium either alone or in combination with N-acetyl cysteine (NAC) against acute mercuric chloride poisoning. The experiment was carried out in male albino Sprague Dawley rats ( n = 30) which was divided into five groups. Group 1 served as control. Groups 2–5 were administered mercuric chloride (HgCl 2: 12 mol/kg, i.p.) once only, group 2 served as experimental control. Animals of groups 3, 4 and 5 were received N-acetyl cysteine (NAC: 0.6 mg/kg, i.p.) and selenium (Se: 0.5 mg/kg, p.o.) and NAC with Se in combination. Acute HgCl 2 toxicity caused significant rise in serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, lactate dehydrogenase, albumin, bilirubin, γ-glutamyl transpeptidase, cholesterol, triglycerides, protein, urea, creatinine, uric acid and blood urea nitrogen content. Animals also showed significantly higher mercury content in liver and kidney, significant rise in lipid peroxidation level with concomitant decrease in reduced glutathione content and the antioxidant enzyme activities of superoxide dismutase and catalase after HgCl 2 exposure. Results of the present investigation clearly showed that combination therapy with NAC + Se provide maximum protection against mercury toxicity than monotherapy (alone treated groups) by preventing oxidative degradation of biological membrane from metal mediated free radical attacks. 相似文献
7.
Manganese (Mn) exposure is related to industrial activities, where absorption by inhalation has high relevance. Manganism, a syndrome caused as a result of excessive accumulation of Mn in the central nervous system, has numerous symptoms similar to those seen in idiopathic Parkinson disease (IPD). Some of these symptoms, such as learning, memory, sensorial, and neurochemical changes, appear before the onset of motor deficits in both manganism and IPD. The aim of this study was to evaluate the possible neuroprotective effects of curcumin against behavioral deficits induced by Mn toxicity in young (2 months old) Swiss mice. We evaluated the effect of chronic inhalation of a Mn mixture [Mn(OAc) 3 and MnCl 2 (20:40 mM)], 1 h/session, three times a week, over a 14-week period on behavioral and neurochemical parameters. Curcumin was supplemented in the diet (500 or 1,500 ppm in food pellets). The Mn disrupted the motor performance evaluated in the single-pellet reach task, as well as the short- and long-term spatial memory evaluated in the step-down inhibitory avoidance task. Surprisingly, curcumin also produced similar deleterious effects in such behavioral tests. Moreover, the association of Mn plus curcumin significantly increased the levels of Mn and iron, and decreased the levels of dopamine and serotonin in the hippocampus. These alterations were not observed in the striatum. In conclusion, the current Mn treatment protocol resulted in mild deficits in motor and memory functions, resembling the early phases of IPD. Additionally, curcumin showed no beneficial effects against Mn-induced disruption of hippocampal metal and neurotransmitter homeostasis. Figure
8.
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
9.
Zuotai (mainly β-HgS) and Zhusha (also called as cinnabar, mainly α-HgS) are used in traditional medicines in combination with herbs or even drugs in the treatment of various disorders, while mercury chloride (HgCl 2) and methylmercury (MeHg) do not have known medical values but are highly toxic. This study aimed to compare the effects of mercury sulfides with HgCl 2 and MeHg on hepatic drug processing gene expression. Mice were orally administrated with Zuotai (β-HgS, 30 mg/kg), α-HgS (HgS, 30 mg/kg), HgCl 2 (33.6 mg/kg), or MeHg (3.1 mg/kg) for 7 days, and the expression of genes related to phase-1 drug metabolism (P450), phase-2 conjugation, and phase-3 (transporters) genes were examined. The mercurials at the dose and duration used in the study did not have significant effects on the expression of cytochrome P450 1–4 family genes and the corresponding nuclear receptors, except for a slight increase in PPARα and Cyp4a10 by HgCl 2. The expressions of UDP-glucuronosyltransferase and sulfotransferase were increased by HgCl 2 and MeHg, but not by Zuotai and HgS. HgCl 2 decreased the expression of organic anion transporter (Oatp1a1), but increased Oatp1a4. Both HgCl 2 and MeHg increased the expression of multidrug resistance-associated protein genes (Mrp1, Mrp2, Mrp3, and Mrp4). Zuotai and HgS had little effects on these transporter genes. In conclusion, Zuotai and HgS are different from HgCl 2 and MeHg in hepatic drug processing gene expression; suggesting that chemical forms of mercury not only affect their disposition and toxicity, but also affect their effects on the expression of hepatic drug processing genes. 相似文献
10.
To evaluate the protective potential of lycopene (Lyc) and proanthocyanidins (PCs) against mercuric chloride (HgCl 2)-induced hepatotoxicity, the study focused on the mechanism of oxidative stress. Firstly, the rats were subcutaneously (s.c.)
injected with 0, 2.2, 4.4, and 8.8 μmol/kg HgCl 2. Additionally, 40 mg/kg Lyc and 450 mg/kg PCs were given to the rats intragastrically (i.g.) before exposure to 8.8 μmol/kg
HgCl 2. Then, body weight, liver weight coefficient, mercury (Hg) contents, histological feature, ultrastructure, apoptosis, reactive
oxygen species (ROS), glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and malondialdehyde
(MDA) in the liver were measured. Lactate dehydrogenase (LDH) and alanine transaminase (ALT) in serum were determined. After
exposure to different concentrations of HgCl 2,it was found that Hg contents, pathological and ultrastructure injury, activities of LDH and ALT, apoptosis, and levels of
ROS, GSH, and MDA increased and the activities of SOD and GSH-Px decreased in a concentration-dependent manner. Further investigation
found that pretreatment with Lyc and PCs inhibited ROS production, protected antioxidant enzymes, and reversed hepatotoxicity.
We concluded that Lyc and PCs had hepatoprotective effects on HgCl 2-induced toxicity by antagonizing oxidative stress in rat liver. 相似文献
11.
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
12.
This study investigated the ability of zinc (Zn) and N-acetylcysteine (NAC) in preventing the biochemical alterations caused by mercury (Hg) and the retention of this metal in different organs. Adult female rats received ZnCl 2 (27 mg/kg) and/or NAC (5 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 after, they were sacrificed and analyses were performed. Hg inhibited hepatic, renal, and blood δ-aminolevulinic acid dehydratase (δ-ALA-D) activity, decreased renal total thiol levels, as well as increased serum creatinine and urea levels and aspartate aminotransferase activity. HgCl 2-exposed groups presented an important retention of Hg in all the tissues analyzed. All pre-treatments demonstrated tendency in preventing hepatic δ-ALA-D inhibition, whereas only ZnCl 2 showed this effect on blood enzyme. Moreover, the combination of these compounds completely prevented liver and blood Hg retention. The exposure to Zn and Hg increased hepatic metallothionein levels. These results show that Zn and NAC presented promising effects against the toxicity caused by HgCl 2. 相似文献
13.
This study investigated the benefits of Cu preexposition on Hg effects on behavioral tests, acetylcholinesterase (AChE) activity and Hg, and essential metal contents in the cerebrum and cerebellum of neonate rats. Wistar rats received (subcutaneous) saline or CuCl 2·2H 2O (6.9 mg/kg/day) when they were 3 to 7 days old and saline or HgCl 2 (5.0 mg/kg/day) when they were 8 to 12 days old. Mercury exposure reduced the performance of rats in the negative geotaxis (3–13 days) and beaker test (17–20 days), inhibited cerebellum AChE activity (13 days), increased cerebrum and cerebellum Hg (13 days), cerebrum Cu (13 days), and cerebrum and cerebellum Zn levels (33 days). The performance of rats in the tail immersion and rotarod tests as well as Fe and Mg levels were not altered by treatments. Copper prevented all alterations induced by mercury. These results are important to open a new perspective of prevention and/or therapy for mercury exposure. 相似文献
14.
When proximal tubule epithelial cells are exposed to HgCl 2, cytoplasmic blebs are formed. These represent on early, potentially reversible response to injury. These blebs are accompanied by reorganization of cytoskeletal proteins, and pre-sumably by alternations in cytoskeletal-plasma membrane interactions. Ca 2+-activated proteinases, such as calpain, are known to affect cytoskeletal proteins and to be involved in diverse cellular processes. However, the role of calpains in cytotoxicity d due to HgCl 2 is unknown. To determine the relationship between Factin, calpain, and HgCl 2 toxicity, cells were stained with fluorescein phalloidin before and after treatment with HgCl 2. Cells were grown on coverslips and exposed to HgCl 2 (10 or 25 M) in the presence or absence of the calpain inhibitor, leupeptin. Untreated cells were flat, polygonal, and contained many fluorescent-stained cables of actin filaments. Generally, cells exposed to HgCl 2 became pleomorphic and contracted as the blebs formed. These cells showed fewer actin cables and fluorescence was seen mostly as either compact areas of dense stain or as peripheral rings. In many cells, actin cables and filaments were completely absent. Disappearance of F-actin was initially seen by 2 min after exposure to HgCl 2. Thus, disruption of the actin cytoskeleton and blebbing were found to be early events in HgCl 2 toxicity. When leupeptin was used with HgCl 2 treatment, the actin staining appeared similar to that of untreated cells. These findings clearly illustrate that HgCl 2 injury to proximal tubule epithelial cells causes rearrangement and alteration of F-actin which may involve the activation of calpain.Abbreviations HgCl 2
mercuric chloride
- PTE
proximal tubule epithelium
- [Ca 2+] i
cytosolic ionized calcium
- [Ca 2+] e
extracellular calcium
- PBS
phosphate buffered saline
Supported by Navy N00014-88-K-0427 & NIH DK15440. This is contribution No. 2905 from the Cellular Pathobiology Laboratory. 相似文献
15.
Mercuric chloride (HgCl 2) has been shown to affect the male reproductive organs, and oxidative stress has been linked with hypospermatogenesis and
with male infertility. However, the specific mode of impairment of spermatogenesis during HgCl 2 exposure has not yet been clarified fully. Because of the involvement of 17β-estradiol (E2) in the male reproductive tract
and its putative role on spermatogenesis, the present study aimed to investigate the possibility that HgCl 2-induced oxidative stress-mediated modulation of the E2 level exerts adverse effects on testicular steroidogenic and gametogenic
activities. HgCl 2 treatment at 50 and 100 ppm for 90 days by continuous oral administration in the drink water resulted in significant dose-dependent
fashion decrease in serum and testicular E 2 levels and an increase in testicular testosterone levels in dose-dependent manner, without statistical alteration in serum
testosterone level among HgCl 2 exposed groups compared to the control. Cauda epididymal sperm count and motility were decreased significantly ( p < 0.01), in a dose-dependent manner, in the HgCl 2-treated groups, and qualitative examination revealed inhibition of spermatogenesis and the preferential loss of maturing
and elongated spermatids. The seminiferous tubules were dilated in treated animals. When compared to the control, increase
in lipid peroxidation due to toxic effects of HgCl2 was accompanied by significant reduction ( p < 0.01) in antioxidant enzymes activities, superoxide dismutase, catalase, and glutathione peroxidase of testes, implicating
the presence of oxidative tissue damage. Furthermore, these tissue injuries caused functional impairment as evidenced with
testicular elevated activity of lactate dehydrogenase. Unless oxidative stress can lead to cancer development, testis’ tumor
markers as beta human chorionic gonadotropin and alpha-fetoprotein levels have shown no significant differences in the HgCl 2-exposed group compared with respect to the control. Large quantities of metal accumulated in the testis tissue are in agreement
with the testis-activity failure verified in this tissue. These findings suggest that a decrease in E2 level after mercury
exposure may render testis more susceptible to oxidative damage leading to its functional inactivation, thus providing new
dimension to mechanisms underlying heavy metal-induced male infertility. 相似文献
16.
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
17.
The neurotoxic effects of aluminum are generally associated with reduced antioxidant capacity, increased oxidative stress and apoptosis, which lead to the induction of neurodegenerative processes. Curcumin has a lipophilic polyphenol character and effects of antioxidant and anti-apoptotic. The present study was undertaken to examine possible aluminum exposure in rats brain synaptosomes and to investigate whether protective and therapeutic effects of curcumin on biochemical and morphological changes in both pre- and post-treated groups. Aluminum chloride (AlCl3) at 50 µM concentration and curcumin at 5 and 10 µg/mL doses were applied to hippocampal synaptosomes of rats according to experimental design. Biochemical effects were evaluated by MTT cytotoxicity, malondialdehyde (MDA) levels, nitric oxide (NO) levels, glutathione (GSH) levels, caspase 3 activities, cytochrome c levels, DNA fragmentation values and protein levels. Morphological examinations were done by TEM analysis. AlCI3 exposure in the synaptosomes enhanced oxidative stress, triggered apoptosis and caused ultrastructural alterations which were well reflected in the TEM images. Curcumin pre-treatment slightly ameliorated the MDA levels, NO levels, cytochrome c levels and caspase 3 activities in AlCI3-exposed synaptosomes, but these results were not statistically significant. Furthermore, curcumin post-treatment significantly improved oxidative damage and morphological alterations, and suppressed cytochrome c and caspase 3 activities. Taken together, our data showed that curcumin had more therapeutic effects than protective effects in AlCI3-induced neurotoxicity. Nevertheless, the therapeutic (post-protective) effects of curcumin should be further investigated in in vivo neurodegenerative models involving behavioral tests. 相似文献
18.
An-Gong-Niu-Huang Wan (AGNH) is a famous traditional Chinese medicine used for brain trauma, hemorrhage, and coma. AGNH contains 10% realgar (As 4S 4) and 10% cinnabar (HgS). Both As and Hg are well-known for their toxic effects, and the safety of AGNH is of concern. To address this question, the acute toxicity of AGNH, realgar and cinnabar were compared to sodium arsenite (NaAsO 2) and mercuric chloride (HgCl 2). Mice were administrated orally AGNH at 1, 3 and 6 g/kg. AGNH at 3 g/kg contains 2.8 mmol As/kg as realgar and 1.18 mmol Hg/kg as cinnabar. Realgar, cinnabar, arsenite (0.28 mmol/kg, 10% of realgar) and HgCl 2 (0.256 mmol/kg, 20% of cinnabar) were orally given to mice for comparison. Blood and tissues were collected 8 h later for toxicity evaluation. Serum alanine aminotransferase was increased by arsenite and blood urea nitrogen was increased by HgCl 2. Total As accumulation after arsenite in liver (100-fold) and kidney (13-fold) was much higher than that after realgar. The accumulation of Hg after HgCl 2 in liver was 400-fold higher and kidney 30-fold higher than after cinnabar. Histopathology showed moderate liver and kidney injuries after arsenite and HgCl 2, but injuries were mild or absent after AGNH, realgar, and cinnabar. The expression of metallothionein-1, a biomarker of metal exposure, was increased 4–10-fold by arsenite and HgCl 2, but was unchanged by AGNH, realgar and cinnabar. Thus, AGNH, realgar and cinnabar are much less toxic acutely than arsenite and HgCl 2. The chemical forms of As and Hg are extremely important factors in determining their disposition and toxicity. 相似文献
19.
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
20.
Lead (Pb) toxicity affects the hepatic and renal systems resulting to homeostasis imbalance. Curcumin is a strong antioxidant but has restrained clinical applications due to its poor bioavailability. Nanomedicine showed promising potentials in drug delivery and has brought forth the use of cockle shell-derived aragonite calcium carbonate nanoparticles (CSCaCO 3NP) to enhance the effectiveness and targeted delivery of curcumin (Cur). Thus, this study aimed at evaluating the therapeutic effect of curcumin-loaded CSCaCO 3NP (Cur- CSCaCO 3NP) on lead-induced hepato-renal toxicity in rats. Thirty-six male adults Sprague-Dawley rats were randomly assigned into five groups. All groups contained six rats each except for group A, which contained 12 rats. All rats apart from the rats in group A (control) were orally administered a flat dose of 50 mg/kg of lead for four weeks. Six rats from group A and B were euthanized after four weeks of lead induction. Oral administration of curcumin (100 mg/kg) for group C and Cur-CSCaCO 3NP (50 and 100 mg/kg) for groups D and E respectively, commenced immediately after 4 weeks of lead induction which lasted for 4 weeks. All rats were euthanized at the 8th week of the experiment. Further, biochemical, histological and hematological analysis were performed. The findings revealed a biochemical, hematological and histological changes in lead-induced rats. However, treatments with the Cur-CSCaCO 3NP and free curcumin reversed the aforementioned changes. Although, Cur-CSCaCO 3NP presented better therapeutic effects on lead-induced toxicity in rats when compared to free curcumin as there was significant improvements in hematological, biochemical and histological changes which is parallel with attenuation of oxidative stress. The findings of the current study hold great prospects for Cur-CSCaCO 3NP as a novel approach for effective oral treatment of lead-induced hepato-renal impairments. 相似文献
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