Blood Δ-aminolevulinic Acid Dehydratase Research Articles

Evaluation of lead exposition length on the liver and intestinal histoarchitecture of eared dove (Zenaida auriculata).

Lead (Pb) is a metal that can produces irreversible damage in living organisms. Some studies had reported that Pb produces histophysiological alterations in the digestive system (mainly liver) of birds; however, the effect of this metal on small intestine has not been fully examined. Additionally, little information is available on Pb disturbances in native birds of South America. The present study aimed to evaluate the effect of different Pb exposure times on blood δ-aminolevulinic acid dehydratase (δ-ALAD) activity and on the histological and morphometric characteristics of the digestive system (liver and proximal intestine) of eared doves (Zenaida auriculata). A decrease of the blood δ-ALAD activity, dilatation of blood vessels and leukocyte infiltrates in intestinal submucosa and muscular layers, and reduction of the enterocyte nuclear diameter and Lieberkühn crypts area were observed. In liver were noted steatosis, proliferation of bile ducts, dilated sinusoids, leukocyte infiltrates, and melanomacrophage centers. The portal tract area and the thickness of the portal vein wall were increased. In conclusion, the results showed that Pb produces histological and morphometric alterations on the liver and small intestine according to the exposure time, which should be considered when the dangerousness of environmental pollutants is evaluated in wild animals.

Does Moringa Oleifera affect element accumulation patterns and lead toxicity in Sprague–Dawley rats?

Moringa Oleifera (MO) has potential for nutritional and medical applications. We verified whether the administration of MO changed mineral accumulation patterns and mitigative effects of lead poisoning using Sprague–Dawley rats. MO leaves, aqueous leaf extracts, and seeds were administrated to rats in two different concentrations (100 and 600 mg/kg body weight/day) for 3 weeks. Element analysis, biochemical blood tests, oxidative-stress assessment, and blood δ-aminolevulinic acid dehydratase (ALAD) activity assays were performed after euthanasia and dissection. Although apparent changes in element accumulation patterns and biochemical parameters for hepatic and renal function assessments were not observed, lead-induced oxidative stress was significantly mitigated by the administration of MO leaves. The administration of high-dose MO leaves and seeds significantly recovered ALAD activity. Further investigations for potential mitigative effects of MO on lead toxicity and its mechanism are required.

Sesamin: Insights into its protective effects against lead-induced learning and memory deficits in rats

BackgroundLead (Pb) is one of the most hazardous pollutants that induce a wide spectrum of neurological changes such as learning and memory deficits. Sesamin, a phytonutrient of the lignan class, exhibits anti-inflammatory, anti-apoptotic, and neuroprotective properties. The present study was designed to investigate the effects of sesamin against Pb-induced learning and memory deficits, disruption of hippocampal theta and gamma rhythms, inflammatory response, inhibition of blood δ-aminolevulinic acid dehydratase (δ-ALA-D) activity, Pb accumulation, and neuronal loss in rats. MethodsSesamin treatment (30 mg/kg/day; P.O.) was started simultaneously with Pb acetate exposure (500 ppm in standard drinking water) in rats, and they continued for eight consecutive weeks. ResultsThe results showed that chronic exposure to Pb disrupted the learning and memory functions in both passive-avoidance and water-maze tests, which was accompanied by increase in spectral theta power and theta/gamma ratio, and a decrease in spectral gamma power in the hippocampus. Additionally, Pb exposure resulted in an enhanced tumor necrosis factor-alpha (TNF-α) content, decreased interleukin-10 (IL-10) production, inhibited blood δ-ALA-D activity, increased Pb accumulation, and neuronal loss of rats. In contrast, sesamin treatment improved all the above-mentioned Pb-induced pathological changes. ConclusionThis data suggests that sesamin could improve Pb-induced learning and memory deficits, possibly through amelioration of hippocampal theta and gamma rhythms, modulation of inflammatory status, restoration of the blood δ-ALA-D activity, reduction of Pb accumulation in the blood and the brain tissues, and prevention of neuronal loss.

Alpha-Lipoic Acid Protects Co-Exposure to Lead and Zinc Oxide Nanoparticles Induced Neuro, Immuno and Male Reproductive Toxicity in Rats.

We evaluated the neuro-, immuno-, and male reproductive toxicity of zinc oxide nanoparticles (ZnO NPs) alone and in combination with lead acetate. We also studied the therapeutic role of α-lipoic acid postexposure. Lead (10 mg/kg, body weight), ZnO NPs (100 mg/kg, bwt) alone, and their combination were administered orally in Wistar rats for 28 days, followed by the administration of α-lipoic acid (15 mg/kg, bwt) for the next 15 days. Our results demonstrated protective effects of α-lipoic acid on lead and ZnO NP–induced biochemical alterations in neurological, immunological, and male reproductive organs in rats. The altered levels of blood δ-aminolevulinic acid dehydratase (ALAD), immunoglobulins (IgA, IgG, IgM, and IgE), interleukins (IL-1β, IL-4, and IL-6), caspase-3, and tumor necrosis factor (TNF-α) were attenuated by lipoic acid treatment. Lead and ZnO NP–induced oxidative stress was decreased by lipoic acid treatment, while a moderate recovery in the normal histoarchitecture of the brain section (cortex and hippocampus) and testes further confirmed the neuro- and male reproductive toxicity of lead and ZnO NPs. We also observed a significant decrease in the blood metal content in the animals treated with lipoic acid compared to the lead-administered group, indicating the moderate chelating property of lipoic acid. It may thus be concluded that lipoic acid might be a promising protective agent against lead and ZnO NP–induced alterations in the neurological, immunological, and reproductive parameters.

Dose-dependent hepatic toxicity and oxidative stress on exposure to nano and bulk selenium in mice.

Selenium is an essential mineral naturally found in soil, water, and some of the food and is required as essential elements in human and animal body. Se supplementation is required especially for those having Se deficiency. Food supplement of selenium has several forms such as selenocysteine, selenite, selenomethionine, and selenate. Recently, Se supplement as selenium nanoparticles (SeNPs) has gained worldwide attention due to its bioactivities and properties. In the present study, we determined the potential hepatotoxicity of nano and bulk selenium using low and high doses in mice. Twenty-five Swiss albino mice (n=5) were randomly divided into 5 groups and treated orally for 28 days: Group 1: sterile saline (0.9%) as a control; Group 2: sodium selenite (1mg/kg); Group 3: sodium selenite (4mg/kg); Group 4: selenium nanoparticles (1mg/kg); and Group 5: selenium nanoparticles (4mg/kg). Administration of nano-selenium (70-90 nm) led to an increase in the activities of serum transaminases (ALT and AST), while no significant effects were noted on biochemical variables indicative of changes in heme synthesis pathway and oxidative stress like blood δ-aminolevulinic acid dehydratase (δ-ALAD), hepatic reactive oxygen species (ROS), catalase activity, superoxide dismutase (SOD), malondialdehyde assay (MDA), reduced glutathione (GSH) and oxidized glutathione (GSSG), glutathione peroxidase (GPx) compared to controls, and a high dose of sodium selenite. Our results suggest that nano-selenium at low dose (1mg/kg) exhibited antioxidant effects in the liver compared to the high dose (4mg/kg) of SeNPs and sodium selenite (1 and 4 mg/kg). The data from the present study might be useful for pharmacologists and toxicologists in providing future directions while designing selenium-based therapeutic strategies.

Comparative efficacy of Nano and Bulk Monoisoamyl DMSA against arsenic-induced neurotoxicity in rats

Chelation therapy is considered as a safe and effective strategy to combat metal poisoning. Arsenic is known to cause neurological dysfunctions such as impaired memory, encephalopathy, and peripheral neuropathy as it easily crosses the blood-brain barrier. Oxidative stress is one of the mechanisms suggested for arsenic-induced neurotoxicity. We prepared Solid Lipid nanoparticles loaded with Monoisoamyl 2, 3-dimercaptosuccinic acid (Nano-MiADMSA), and compared their efficacy with bulk MiADMSA for treating arsenic-induced neurological and other biochemical effects. Solid lipid nanoparticles entrapping MiADMSA were synthesized and particle characterization was carried out by transmission electron microscopy (TEM) and dynamic light scattering (DLS). An in vivo study was planned to investigate the therapeutic efficacy of MiADMSA-encapsulated solid lipid nanoparticles (Nano-MiADMSA; 50 mg/kg orally for 5 days) and compared it with bulk MiADMSA against sodium meta-arsenite exposed rats (25 ppm in drinking water, for 12 weeks) in male rats. The results suggested the size of Nano-MiADMSA was between 100−120 nm ranges. We noted enhanced chelating properties of Nano-MiADMSA compared with bulk MiADMSA as evident by the reversal of oxidative stress variables like blood δ-aminolevulinic acid dehydratase (δ-ALAD), Reactive Oxygen Species (ROS), Catalase activity, Superoxide Dismutase (SOD), Thiobarbituric Acid Reactive Substances (TBARS), Reduced Glutathione (GSH) and Oxidized Glutathione (GSSG), Glutathione Peroxidase (GPx), Glutathione-S-transferase (GST) and efficient removal of arsenic from the blood and tissues. Recoveries in neurobehavioral parameters further confirmed nano-MiADMSA to be more effective than bulk MiADMSA. We conclude that treatment with Nano-MiADMSA is a better therapeutic strategy than bulk MiADMSA in reducing the effects of arsenic-induced oxidative stress and associated neurobehavioral changes.

Effect of sub-chronic exposure to lead (Pb) and Bacillus subtilis on Carassius auratus gibelio: Bioaccumulation, antioxidant responses and immune responses

Lead (Pb) poisoning in humans and fish represents a significant global problem. Bacillus subtilis (B. subtilis) is a widely used probiotic in aquaculture. Carassius auratus gibelio (C. gibelio) is one of the most important aquaculture species with great commercial value. The objective of this study was to evaluate the potential of B. subtilis in ameliorating lead-induced toxicity in C. gibelio. The fish were exposed for 60 days to waterborne Pb at 0, 0.05, 0.5 and 1 mg/L and/or dietary B. subtilis at 109 cfu/g. After 30 and 60 days, the fish were sampled and bioaccumulation, antioxidant activity and immune responses were assessed. The results revealed that B. subtilis confers significant protective effects against lead toxicity by preventing alterations in the levels of bioaccumulation, superoxide dismutase, catalase and glutathione. B. subtilis also assists in the recovery of blood δ-aminolevulinic acid dehydratase, lysozyme, and IgM levels while regulating the expression of immune-related genes including IL-10, lysozyme, TNF-α, IgM and Hsp70 after 60 days of lead exposure. Our results suggest that administration of B. subtilis (109 cfu/g) has the potential to combat lead toxicity in C. gibelio.

Dietary Lactobacillus plantarum supplementation decreases tissue lead accumulation and alleviates lead toxicity in Nile tilapia (Oreochromis niloticus )

Pollution by the heavy metal lead (Pb) has become a threat to both aquaculture and food safety. In this study, the protective effects of a selected probiotic with good Pb binding capacity (Lactobacillus plantarumCCFM8661) against waterborne Pb exposure were evaluated in Nile tilapia (Oreochromis niloticus). One hundred and eighty fish were divided into four groups as control, Pb-only, Pb-plus-CCFM8661 and CCFM8661-only. Fish were exposed to a dose of waterborne Pb level at 1 mg L−1 for 4 weeks, and the probiotic was administered at 108 CFU g−1 in fish diet twice daily. The results showed that dietary supplementation of CCFM8661 ameliorated the growth performance and prevented the death of Pb-exposed fish. Cotreatment with Pb and CCFM8661 also effectively decreased Pb accumulation in kidney, liver, gonad, brain, gills and muscle. Moreover, the administration of this probiotic alleviated Pb-induced oxidative stress, recovered digestive enzyme activities and blood δ-aminolevulinic acid dehydratase activity, reversed alterations in innate immune status and decreased the frequencies of the nuclear abnormalities in peripheral blood erythrocytes of fish. These results suggested that CCFM8661 may be a novel dietary supplement against Pb toxicity at least in tilapia.

Effects of sub-lethal and chronic lead concentrations on blood and liver ALA-D activity and hematological parameters in Nile tilapia

Liver and blood δ-aminolevulinic acid dehydratase (ALA-D) inhibition by exposure to sub-lethal lead concentrations over time in Nile tilapia (Oreochromis niloticus) were investigated. All three lead concentrations (1mgkg−1, 10mgkg−1 and 100mgkg−1) significantly inhibited ALA-D activity in blood (319±29.2; 180±14.6 and 172±19µmols−1h−1L−1 respectively) and liver (302±5.84; 201±41.4 and 93±22.1µmols−1h−1L−1) 24h after injection relative to controls (blood: 597±37.0µmols−1h−1L−1; liver: 376±23.1µmols−1h−1L−1). Blood ALA-D was greatly inhibited in all but the highest lead dose. Fish were then exposed to 1mgkg−1 lead for 9 days, and presented short-term hyperglycemia, decreased hemoglobin and hematocrit values and time-dependent blood ALA-D activity inhibition, corroborating blood ALA-D activity as being more suitable for investigating lead effects, showing dose and time-dependent ALA-D inhibition after lead exposure. The results of the present study also demonstrated that fish size affects blood ALA-D activity, as fish from the 24-h assay, which were slightly smaller (approximately 200g), showed higher ALA-D inhibition in response to lead exposure when compared to the fish from the 9-day assay (approximately 500g). Thus, fish size should always be taken into account both in the field and in laboratory settings, and efforts should be made to obtain uniform fish size samples for biomarker studies.

Antioxidant protection of gallic acid against toxicity induced by Pb in blood, liver and kidney of rats.

The effect of the antioxidant gallic acid (GA) on Pb toxicity in blood, liver and kidney was investigated in the present study. Rats Wistar received Pb nitrate (50 mg/Kg/day, i.p., 5 days) followed by GA (13.5 mg/Kg, p.o., 3 days) or a chelating agent (EDTA, 55 mg/Kg, i.p.). As result, Pb decreased body weight, hematocrit and blood δ-aminolevulinic acid dehydratase (ALA-D) activity. In addition, high Pb levels were observed in blood and tissues, together with increased (1) lipid peroxidation in erythrocytes, plasma and tissues, (2) protein oxidation in tissues and (3) plasma aspartate transaminase (AST) levels. These changes were accompanied by decreasing in antioxidant defenses, like superoxide dismutase (SOD) activity in tissues and catalase (CAT) activity and reduced glutathione (GSH) in liver. GA was able to reverse Pb-induced decrease in body weight and ALA-D activity, as well as Pb-induced oxidative damages and most antioxidant alterations, however it did not decrease Pb bioaccumulation herein as EDTA did. Furthermore, EDTA did not show antioxidant protection in Pb-treated animals as GA did. In conclusion, GA decreased Pb-induced oxidative damages not by decreasing Pb bioaccumulation, but by improving antioxidant defenses, thus GA may be promising in the treatment of Pb intoxications.

Zinc and N-acetylcysteine modify mercury distribution and promote increase in hepatic metallothionein levels

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 ZnCl2 (27mg/kg) and/or NAC (5mg/kg) or saline (0.9%) subcutaneously and after 24h they received HgCl2 (5mg/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. HgCl2-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 ZnCl2 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 HgCl2.

The influence of gingerol treatment on aluminum toxicity in rats.

Ginger is widely used as a medicine in the Ayurvedic system. It contains the active compound gingerol, which scavenges free radicals. Prolonged intake of aluminum (Al) in drinking water and from other sources may lead to neurological, renal, and hepatic dysfunction. The present study was designed to evaluate the protective effect of gingerol, an active principal of ginger against aluminum as Al (NO3)3 -induced toxicity in rats. Al (NO3)3 at 32.5 mg/kg body weight was administered to female albino rats intraperitoneally once only, followed by treatment with gingerol at 25, 50, and 100 mg/kg p.o. for 3 consecutive days beginning 24 h after Al exposure. Animals of all of the groups were sacrificed after 48 h of the last gingerol treatment for experimental observations. Significant elevations were observed in serum tranaminases, cholesterol, triglyceride, creatinine, urea, and blood δ-aminolevulinic acid dehydratase (ALAD) after Al exposure. In liver, kidney, and brain tissues, the thiobarbituric acid reactive substances (TBARS) level and total and esterified cholesterol were significantly increased, whereas glutathione (GSH), acetyl cholinesterase (AChE), and δ-aminolevulinic acid synthetase (ALAS) were significantly decreased. Treatment of gingerol for 3 days surprisingly reversed almost all of the biochemical variables toward control levels in a significant manner. Treatment with gingerol (50 mg/kg body weight) was most effective in coping with aluminum-induced toxicity in rats. The antioxidant activity of gingerol might be due not only to the radical scavenging activity of antioxidants but also to the affinity of these antioxidants to the substrates.

Effectiveness of (PhSe)2 in protect against the HgCl2 toxicity

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 (HgCl2). Selenium (Se) and mercury (Hg) determination was also carried out. Mice received a daily oral dose of (PhSe)2 (5.0mg/kg/day) or canola oil for five consecutive days. During the following five days, the animals were treated with a daily subcutaneous dose of HgCl2 (5.0mg/kg/day) or saline (0.9%). Twenty-four hours after the last HgCl2 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 HgCl2 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.

Efficacy of some antioxidants supplementation in reducing oxidative stress post sodium tungstate exposure in male wistar rats

This study aimed to evaluate the protective efficacy of some antioxidants against sodium tungstate induced oxidative stress in male wistar rats. Animals were sub-chronically exposed to sodium tungstate (100ppm in drinking water) for three months except for control group. In the same time, many rats were supplemented orally with different antioxidants (alpha-lipoic acid (ALA), n-acetylcysteine (NAC), quercetin or naringenin (0.30mM)) for five consecutive days a week for the same mentioned period before. Exposure to sodium tungstate significantly (P<0.05) inhibit blood δ-aminolevulinic acid dehydratase (ALAD) activity, liver and blood reduced glutathione (GSH) levels and an increase in oxidized glutathione (GSSG) and thiobarbituric acid reactive species (TBARS) levels in tissues. ALA acid and NAC supplementation post sodium tungstate exposure increased GSH and also, was beneficial in the recovery of altered superoxide dismutase and catalase activity, besides, significantly reducing blood and tissue reactive oxygen species and TBARS levels. The results suggest a more pronounced efficacy of ALA acid and NAC supplementation than quercetin or naringenin supplementation post sodium tungstate exposure in preventing induced oxidative stress in rats.

Metal Accumulation, Blood δ-Aminolevulinic Acid Dehydratase Activity and Micronucleated Erythrocytes of Feral pigeons (Columba Livia) Living Near Former Lead-Zinc Smelter “ Trepça” – Kosovo

The concentration of lead in blood and tibia (Pb), zinc (Zn) and cupper (Cu) in tibia, blood δ - aminolevulinic acid dehydratase (ALA-D; EC: 4.2.1.24) activity, hematocrit value (Hct) and micronuclei frequency (MN) of peripheral erythrocytes have been determinated in three different populations of feral pigeons (Columba livia; forma urbana and forma domestica), collected in Mitrovica town (situated close to smelter Trepca, down closed in 2000 year ) and in rural area (Koshare willage ) . The blood lead level in feral pigeons from Mitrovica (forma urbana) was 3 times higher (149.6; 50.5 µg%) in comparison with that in feral pigeons from Mitrovica (forma domestica) and 27.7 times higher (5.4 µg% in comparison with pigeons from rural area. The Pb concentration of tibia of feral pigeons (froma urbana and forma domestica), from Mitrovica town was significantly higher (P<0.001) in comparison with control. The concentration of Zn in tibia of feral pigeons from Mitrovica town (forma urbana), was significantly higher (P<0.006) in comparison with control. The blood ALA-D activity of feral pigeons from Mitrovica town (forma urbana and froma domestica), was significantly inhibited in comparison with control. The blood ALA-D activity of feral pigeons -forma urbana from Mitrovica town was significantly inhibited (P<0.001) in comparison with the blood ALA-D activity of feral pigeons-forma domestica from Mitrovica town. The erythrocyte MN frequency of feral pigeons from Mitrovica was significantly higher (P <0.001) in comparison with controls. The smelter Trepca ten year after closed down pose a threat to the local environment, biota and people's health.

Diphenyl ditelluride targets brain selenoproteins in vivo: inhibition of cerebral thioredoxin reductase and glutathione peroxidase in mice after acute exposure

In this study, we investigated the effect of diphenyl ditelluride (PhTe)(2) administration (10 and 50 μmol/kg) on adult mouse behavioral performance as well as several parameters of oxidative stress in the brain and liver. Adult mice were injected with (PhTe)(2) or canola oil subcutaneously (s.c.) daily for 7 days. Results demonstrated that (PhTe)(2) induced prominent signs of toxicity (body weight loss), behavioral alterations and increased in lipid peroxidation in brain. 50 μmol/kg (PhTe)(2) inhibited blood δ-aminolevulinic acid dehydratase (δ-ALA-D), a redox sensitive enzyme. (PhTe)(2) caused an increase in cerebral non-protein thiol (NPSH) and protein thiol (PSH) groups. In the liver, 50 μmol/kg (PhTe)(2) decreased NPSH, but did not alter the content of protein thiol groups. (PhTe)(2) decreased cerebral antioxidant enzymes (catalase (CAT), superoxide dismutase (SOD), glutathione reductase (GR), glutathione peroxidase (GPx), and thioredoxin reductase (TrxR). In liver, (PhTe)(2) increase SOD and GR and decreased GPx activity. Results obtained herein suggest that the brain was more susceptible to oxidative stress induced by (PhTe)(2) than the liver. Furthermore, we have demonstrated for the first time that TrxR is an in vivo target for (PhTe)(2.) Combined, these results highlight a novel molecular mechanism involved in the toxicity of (PhTe)(2). In particular the inhibition of important selenoenzymes (TrxR and GPx) seems to be involved in the neurotoxicity associated with (PhTe)(2) exposure in adult mice.

Curcumin encapsulated in chitosan nanoparticles: A novel strategy for the treatment of arsenic toxicity

Water-soluble nanoparticles of curcumin were synthesized, characterized and applied as a stable detoxifying agent for arsenic poisoning. Chitosan nanoparticles of less than 50nm in diameter containing curcumin were prepared. The particles were characterized by TEM, DLS and FT-IR. The therapeutic efficacy of the encapsulated curcumin nanoparticles (ECNPs) against arsenic-induced toxicity in rats was investigated. Sodium arsenite (2mg/kg) and ECNPs (1.5 or 15mg/kg) were orally administered to male Wistar rats for 4weeks to evaluate the therapeutic potential of ECNPs in blood and soft tissues. Arsenic significantly decreased blood δ-aminolevulinic acid dehydratase (δ-ALAD) activity, reduced glutathione (GSH) and increased blood reactive oxygen species (ROS). These changes were accompanied by increases in hepatic total ROS, oxidized glutathione, and thiobarbituric acid-reactive substance levels. By contrast, hepatic GSH, superoxide dismutase and catalase activities significantly decreased on arsenic exposure, indicative of oxidative stress. Brain biogenic amines (dopamine, norepinephrine and 5-hydroxytryptamine) levels also showed significant changes on arsenic exposure. Co-administration of ECNPs provided pronounced beneficial effects on the adverse changes in oxidative stress parameters induced by arsenic. The results indicate that ECNPs have better antioxidant and chelating potential (even at the lower dose of 1.5mg/kg) compared to free curcumin at 15mg/kg. The significant neurochemical and immunohistochemical protection afforded by ECNPs indicates their neuroprotective efficacy. The formulation provides a novel therapeutic regime for preventing arsenic toxicity.

Lactobacillus plantarum CCFM8661 Alleviates Lead Toxicity in Mice

Lead causes a broad range of adverse effects in humans and animals. The objective was to evaluate the potency of lactobacilli to bind lead in vitro and the protective effects of a selected Lactobacillus plantarum CCFM8661 against lead-induced toxicity in mice. Nine strains of bacteria were used to investigate their binding abilities of lead in vitro, and L. plantarum CCFM8661 was selected for animal experiments because of its excellent lead binding capacity. Both living and dead L. plantarum CCFM8661 were used to treat 90 male Kunming mice during or after the exposure to 1g/L lead acetate in drinking water. The results showed oral administration of both living and dead L. plantarum CCFM8661 offered a significant protective effect against lead toxicity by recovering blood δ-aminolevulinic acid dehydratase activity, decreasing the lead levels in blood and tissues, and preventing alterations in the levels of glutathione, glutathione peroxidase, malondialdehyde, superoxide dismutase, and reactive oxygen species caused by lead exposure. Moreover, L. plantarum CCFM8661 was more effective when administered consistently during the entire lead exposure, not after the exposure. Our results suggest that L. plantarum CCFM8661 has the potency to provide a dietary strategy against lead toxicity.

Dose-Dependent Effects of Ethanol on Lead-Induced Oxidative Stress in Rats

This study explored the dose-dependent effects of ethanol ingestion during co-exposure with lead in rats. Lead was administered orally, once daily at a dose of 10 mg/kg whereas ethanol was given in drinking water at 3 different doses: 1%, 2%, and 5% along with lead. The exposure continued for 3 months, after which the animals were decapitated and various biochemical assays were carried out. The results show increased oxidative stress in animals co-exposed to lead and ethanol compared with either lead or ethanol alone. A significant decrease in blood δ-aminolevulinic acid dehydratase activity, glutathione (GSH), GSH peroxidase, adenosine triphosphatase, and catalase but a significant increase in reactive oxygen species, oxidized GSH, thiobarbituric acid reactive substance, and intracellular calcium was noted in lead and ethanol co-exposed animals. The changes were found to be dose dependent in lead plus ethanol exposed animals. Decrease in glucose-6-phosphate dehydrogenase activity in blood was noted, with no significant changes in liver and kidney. Aldehyde dehdrogenase activity decreased significantly in animals exposed to either lead or ethanol but a pronounced depletion was seen in rats co-exposed to lead and ethanol (5%). The results suggest that the combined exposure to lead and ethanol leads to increased oxidative stress and possible initiation of apoptosis in rats.

Influence of chelating therapy against aluminum chloride-induced immune suppression and hematological disorders in rabbits

This study aimed to evaluate the capability of chelating therapy in reducing the immunotoxic and hematotoxic effects induced by aluminum chloride (AlCl3). For this purpose, 40 male, adult, New Zealand white rabbits were divided into four groups with 10 animals each [control, AlCl3, and hydroxyethyl-ethylene diaminetriacetic acid (HEDTA) or Tiron plus AlCl3 groups]. Aluminum chloride administered via drinking water in a dose of 20 mg/l for 3 months. After that HEDTA or Tiron was administered i.p. at a dose of 50 and 471 mg/kg b.w., respectively, for 21 days, three times/week. Aluminum chloride-exposed rabbits showed a significant decrease in the number of red blood cells, blood hemoglobin concentration, and hematocrit value. Blood δ-aminolevulinic acid dehydratase activity and heme concentration showed a significant decrease than the control group. Serum IgA, IgG, and IgM levels were also significantly lower in AlCl3-exposed group than control. A prominent exhaustion of lymphoid elements of all investigated lymphoid organs was obtained. Histochemical enzymatic detection revealed weak positive nonspecific esterase or alkaline phosphatase staining reaction in macrophages, T and B lymphocytes, respectively, in AlCl3-exposed group in comparison of strong staining reaction in the control group. The present results indicated that long-term oral exposure to low doses of AlCl3 promotes alterations on hematological indices and some immune parameters in rabbits. In addition, most of the above parameters responded positively with Tiron or HEDTA chelating therapy but the effectiveness of Tiron therapy is more pronounced.