Δ-aminolevulinic Acid Dehydratase Activity Research Articles

Organoselenium Bis Selenide Attenuates 3-Nitropropionic Acid-Induced Neurotoxicity in Rats

This study was designed to evaluate the effects of bis selenide on Huntington disease (HD)-like signs induced by 3-nitropropionic acid (3-NP) in rats. To this aim, rats were treated for 4days with bis selenide (5 or 20mg/kg/day, per oral) 30min before 3-NP (20mg/kg/day, intraperitoneally). The body weight gain, locomotor activity, motor coordination, and biochemical parameters in striatal preparations were assessed 24h after the last injection of 3-NP. The highest dose of bis selenide was effective in protecting against body weight loss and motor coordination deficit induced by 3-NP. The impairment of locomotor activity caused by 3-NP was abolished by bis selenide at both doses. Bis selenide (5 and 20mg/kg) partially restored succinate dehydrogenase activity inhibited after 3-NP exposure. The dose of 20mg/kg of bis selenide recovered partially δ-aminolevulinic acid dehydratase activity, and totally Na(+), K(+)-ATPase activity, two sulfhydryl enzymes sensitive to oxidizing agents, which had their activities inhibited by 3-NP. Also, 3-NP led to an increase in protein carbonyl levels and glutathione reductase activity and inhibited catalase activity-alterations that were reversed by bis selenide administration at both doses. The highest dose of bis selenide was effective against the increase of RS levels, the depletion of reduced glutathione content, and the inhibition of glutathione peroxidase activity induced by 3-NP. Bis selenide was not effective against inhibition of SOD activity caused by 3-NP. These findings demonstrate that bis selenide elicited protective effects against HD-like signs induced by 3-NP in rats.

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.

Genotoxic effects of occupational exposure to lead and influence of polymorphisms in genes involved in lead toxicokinetics and in DNA repair

Lead is still widely used in many industrial processes and is very persistent in the environment. Although toxic effects caused by occupational exposure to lead have been extensively studied, there are still conflicting results regarding its genotoxicity. In a previous pilot study we observed some genotoxic effects in a population of lead exposed workers. Thus, we extended our study analysing a larger population, increasing the number of genotoxicity endpoints, and including a set of 20 genetic polymorphisms related to lead toxicokinetics and DNA repair as susceptibility biomarkers. Our population comprised 148 workers from two Portuguese factories and 107 controls. The parameters analysed were: blood lead levels (BLL) and δ-aminolevulinic acid dehydratase (ALAD) activity as exposure biomarkers, and T-cell receptor (TCR) mutation assay, micronucleus (MN) test, comet assay and OGG1-modified comet assay as genotoxicity biomarkers. Lead exposed workers showed markedly higher BLL and lower ALAD activity than the controls, and significant increases of TCR mutation frequency (TCR-Mf), MN rate and DNA damage. Oxidative damage did not experience any significant alteration in the exposed population. Besides, significant influence was observed for VDR rs1544410 polymorphism on BLL; APE1 rs1130409 and LIG4 rs1805388 polymorphisms on TCR-Mf; MUTYH rs3219489, XRCC4 rs28360135 and LIG4 rs1805388 polymorphisms on comet assay parameter; and OGG1 rs1052133 and XRCC4 rs28360135 polymorphisms on oxidative damage. Our results showed genotoxic effects related to occupational lead exposure to levels under the Portuguese regulation limit of 70μg/dl. Moreover, a significant influence of polymorphisms in genes involved in DNA repair on genotoxicity biomarkers was observed.

Exposure to Low Level of Arsenic and Lead in Drinking Water from Antofagasta City Induces Gender Differences in Glucose Homeostasis in Rats

Populations chronically exposed to arsenic in drinking water often have increased prevalence of diabetes mellitus. The purpose of this study was to compare the glucose homeostasis of male and female rats exposed to low levels of heavy metals in drinking water. Treated groups were Sprague-Dawley male and female rats exposed to drinking water from Antofagasta city, with total arsenic of 30 ppb and lead of 53 ppb for 3 months; control groups were exposed to purified water by reverse osmosis. The two treated groups in both males and females showed arsenic and lead in the hair of rats. The δ-aminolevulinic acid dehydratase was used as a sensitive biomarker of arsenic toxicity and lead. The activity of δ-aminolevulinic acid dehydratase was reduced only in treated male rats, compared to the control group. Treated males showed a significantly sustained increase in blood glucose and plasma insulin levels during oral glucose tolerance test compared to control group. The oral glucose tolerance test and the homeostasis model assessment of insulin resistance demonstrated that male rats were insulin resistant, and females remained sensitive to insulin after treatment. The total cholesterol and LDL cholesterol increased in treated male rats vs. the control, and triglyceride increased in treated female rats vs. the control. The activity of intestinal Na+/glucose cotransporter in male rats increased compared to female rats, suggesting a significant increase in intestinal glucose absorption. The findings indicate that exposure to low levels of arsenic and lead in drinking water could cause gender differences in insulin resistance.

Amelioration of aluminium induced toxicity by Allium sativum

Garlic (Allium sativum L., Liliaceae) is a nature’s boon to mankind, which has played an important dietary and therapeutic medicinal role throughout the history of mankind. Aluminum (Al) is a potent neurotoxin and has been associated with Alzheimer's disease causality for decades. The study aims to demonstrate the ameliorative effect of garlic extract against aluminium-induced toxicity in rat model. Animals received aluminium nitrate 32.5 mg/kg (1/2 LD50 of Al (NO3)3 i.p.) once only. Different doses of garlic extract (25, 50 and 100 mg/kg) was administered for 3 days after 24 h of Al exposure. The activity of AChE was inhibited in all the parts of the brain, significant rise was observed in the activities of serum LDH, AST and ALT whereas serum protein was declined after toxicant exposure. The activity of δ-aminolevulinic acid dehydratase in blood and δ-aminolevulinic acid synthetase in brain depicted fall after Al exposure. Al provoked significant increase in the level of cholesterol, triglyceride, creatinine and urea level in serum. TBARS level, total and esterified cholesterol in liver, kidney and brain were significantly higher with concomitant fall in reduced glutathione content during toxicity. Garlic markedly attenuated oxidative stress by scavenging various free radicals significantly restored the deranged biochemical variables. Histopathological changes in liver, kidney and brain were also recouped and biochemical findings substantiated. Results of present study concluded that garlic can counteract the deleterious effects of aluminium. Key words: Garlic extract, aluminium, oxidative stress, liver, kidney, brain.

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.

Age dependent changes in arsenic and nicotine induced oxidative stress in male rat

Abstract The present study was planned to compare the differential toxicity of arsenic and nicotine among three different age groups of rats. In this study blood and tissue oxidative stress was determined in different age group of rats exposed to arsenic (2 mg/kg, i.p.) and nicotine (6 mg/kg, i.p.) for 2 weeks. Arsenic inhibited blood δ-aminolevulinic acid dehydratase activity in all age groups of rats while, a moderate inhibition was noted following nicotine exposure in young and old rats. Arsenic caused an increase in blood reactive oxygen species in young and old rats while glutathione level increased only in young rats unlike nicotine. A significant increase in thiobarbituric acid reactive substance was noted in liver of young and old rats while, hepatic GSH showed an increase in young and a decrease in old rats. Catalase activity decreased significantly in arsenic exposed young and old rats. At the given dose and duration both toxicants did not induce oxidative stress in rat brain. Blood arsenic concentration increased with age whereas its level brain and liver was independent of age. Conclusively, young and old animals were found to be most sensitive to both toxicants; with arsenic being more toxic than nicotine targeting liver.

Mutagenic, genotoxic and enzyme inhibitory effects of carbosulfan in rainbow trout Oncorhynchus mykiss

Rainbow trout ( Oncorhynchus mykiss; 116.88 ± 21.69 g) were exposed to sublethal concentrations (25 μg/L) of carbosulfan for 60 days to test if the long term exposure of fish to carbosulfan affects red blood cells acetylcholinesterase (AChE), δ-aminolevulinic acid dehydratase (ALA-D) and paraoxonase (PON) enzyme activity and induces genotoxic and/or mutagenic effects. The exposure resulted in inhibition of AChE and ALA-D activity of rainbow trout when compared to control fish. The activity of PON was not affected by carbosulfan. Interestingly, carbosulfan was found to induce DNA damage in red blood cells (comet assay) and proved to be mutagenic as revealed by the Ames test. Results indicate that blood AChE and ALA-D of rainbow trout may be a sensitive biomarker for assessment of carbosulfan contaminated water bodies. Furthermore, because the Ames test and comet assay were proven successful to detect the genotoxicity of carbosulfan, we proposed that nonlethal techniques such as blood collection from caudal vein of fish should be used to determine potential toxic effects of other pesticides to surrounding environment.

Blood Pb and δ-ALAD inhibition in cattle and sheep from a Pb-polluted mining area

The effects of Pb pollution on cattle and sheep raised in an ancient mining area were studied through the use of blood Pb (PbB) levels and δ-aminolevulinic acid dehydratase (δ-ALAD) activity. Lead levels in livestock blood from the mining area ( n = 110) were significantly elevated when compared to the controls ( n = 79). In 91.4% of cattle ( n = 58) and 13.5% of sheep ( n = 52) sampled in the mining area, PbB levels corresponded to subclinical exposure (6–35 μg/dl). Two young cattle (<2 years) from the mining area ( n = 5) had PbB levels indicative of clinical poisoning (>35 μg/dl). Elevated PbB was also accompanied by δ-ALAD activity inhibition in blood, which confirms that measurable effects of Pb poisoning were taking place. Observed PbB levels suggest that a potential risk to human consumers of beef from the Pb polluted areas may also exist, as has been shown previously for game meat from the same mining area.

Effects of lead on the growth, lead accumulation and physiological responses of Pluchea sagittalis

This work aimed to study the process of stress adaptation in root and leaves of different developmental stages (apex, middle and basal regions) of Pluchea sagittalis (Lam.) Cabrera plants grown under exposure to five Pb levels (0, 200, 400, 600 and 1000μM) for 30days. Pb concentration and content in roots, stems, and leaves of different developmental stages increased with external Pb level. Consumption of nutrient solution, transpiration ratio, leaf fresh weight, leaf area, and shoot length decreased upon addition of Pb treatments. However, dry weight of shoot parts and roots did not decrease upon addition of Pb treatments. Based on index of tolerance, the roots were much more tolerant to Pb than shoots. δ-aminolevulinic acid dehydratase activity was decreased by Pb treatments, whereas carotenoid and chlorophyll concentrations were not affected. Lipid peroxidation and hydrogen peroxide concentration both in roots and leaves increased with increasing Pb levels. Pb treatments increased ascorbate peroxidase activity in all plant parts, while superoxide dismutase activity increased in leaves and did not change in roots. Catalase activity in leaves from the apex shoot was not affected by Pb, but in other plant parts it was increased. Pb toxicity caused increase in non-protein thiol groups concentration in shoot parts, whereas no significant difference was observed in roots. Both root and shoot ascorbic acid concentration increased with increasing Pb level. Therefore, it seems that Pb stress triggered an efficient defense mechanism against oxidative stress in P. sagittalis but its magnitude was depending on the plant organ and of their physiological status. In addition, these results suggest that P. sagittalis is Pb-tolerant. In conclusion, P. sagittalis is able to accumulate on average 6730 and 550μg Pb g(-1) dry weight, respectively, in the roots and shoot, a physiological trait which may be exploited for the phytoremediation of contaminated soils and waters.

Lead exposure and poisoning of songbirds using the Coeur d'Alene River Basin, Idaho, USA

Previous studies have found widespread Pb poisoning of waterfowl in the Coeur d'Alene River Basin in northern Idaho, USA, which has been contaminated by mining and smelting activities. We studied the exposure of ground-feeding songbirds to Pb, sampling 204 American robins (Turdus migratorius), song sparrows (Melospiza melodia), and Swainson's thrushes (Catharus ustulatus) throughout the basin. These songbirds had mean blood Pb concentrations (mg/kg, dry weight) of less than 0.19 at a reference area (25 mg Pb/kg soil), 1.09 at moderately contaminated sites (170 to 1300 mg Pb/kg soil), and 2.06 at highly contaminated sites (2000 to 5000 mg Pb/kg soil). Based on guidelines for evaluating blood Pb in birds, 6% of robins from the highly contaminated sites had background concentrations, 24% were subclinically poisoned, 52% were clinically poisoned, and 18% were severely clinically poisoned with Pb. Blood Pb concentrations were lower in song sparrows than in robins and lowest in Swainson's thrushes. More than half of the robins and song sparrows from all contaminated sites and more than half of the Swainson's thrushes from highly contaminated sites showed at least 50% inhibition of the activity of the enzyme δ-aminolevulinic acid dehydratase (ALAD), commonly used as a measure of exposure to Pb. The highest hepatic Pb concentration of 61 mg/kg (dry weight) was detected in a song sparrow. Using Al as a marker for soil in songbird ingesta, we estimated average soil ingestion rates as 20% in robins, 17% in song sparrows, and 0.7% in Swainson's thrushes. Soil Pb in ingesta accounted for almost all of the songbirds' exposure to Pb. Based on these results, it is recommended that ecological risk assessments of ground-feeding songbirds at contaminated sites include soil ingestion as a pathway of exposure to Pb.

Inhibition of δ-aminolevulinic acid dehydratase activity by cadmium in excised etiolated maize leaf segments during greening

Supply of 0.1&amp;ndash;0.5 mmol CdCl&lt;sub&gt;2&lt;/sub&gt; inhibited &amp;delta;-aminolevulinic acid dehydratase (EC 4.2.1.24, ALAD) activity and total chlorophylls in excised etiolated segments of maize leaves during greening. Due to cadmium supply &amp;delta;-aminolevulinic acid (ALA) content was reduced significantly at 0.5 mmol Cd only. Also the Cd treatment decreased the protein content and accumulated significantly the Cd in the tissue. Significant correlation between Cd accumulation in the leaves and various parameters measured is observed, with the R-squared values being 0.727 with ALAD activity, 0.885 with ALA content, 0.902 with total chlorophylls and 1.00 with proteins. The % inhibition of ALAD activity by Cd was decreased in the presence of nitrogenous compounds, glutamine and NH&lt;sub&gt;4&lt;/sub&gt;NO&lt;sub&gt;3&lt;/sub&gt; and the observed inhibition was 25% and 16%, respectively. More substantial reduction in % inhibition of enzyme activity by Cd was observed during treatment with glutathione, a ubiquitous thiol and levulinic acid, a competitive inhibitor of ALAD, with the inhibition being only 2% and 4%, respectively. Supply of some essential metal ions, such as Mg, Zn, and Mn, also reduced the % inhibition of enzyme activity by Cd. Inclusion of varying concentrations of ALA during assay also affected the % inhibition of enzyme activity by Cd showing an increased inhibition from 17% to 53% with increasing ALA concentration. It is suggested that Cd inhibits ALAD activity by affecting the ALA binding to the enzyme and/or disrupting thiol interaction.

Zinc alleviates mercury-induced oxidative stress in Pfaffia glomerata (Spreng.) Pedersen

The possible role of zinc (Zn) to reverse the oxidative stress caused by mercury (Hg) was investigated in Pfaffia glomerata plantlets. Thirty-day-old acclimatized plantlets of P. glomerata were exposed to four treatments: control, 50 μM Zn, 50 μM Hg and 50 μM Zn + 50 μM Hg for 9 days. In Zn + Hg treatment, shoot and root Hg concentrations were 59 and 24% smaller than that plants exposed to 50 μM Hg added alone. An increase in the Zn concentration in the shoot of plants exposed to Zn + Hg occurred, although in the roots Zn concentration was not altered, when compared to the control. Fresh and dry weights, as well as the activity of δ-aminolevulinic acid dehydratase (δ-ALA-D) in Hg-treated plants were significantly reduced. Percentage survival, fresh and dry weights and δ-ALA-D activity of plants treated by 50 μM Zn + 50 μM Hg were greater than of that treated by Hg alone. Moreover, Zn treatment reduced the lipid peroxidation caused by Hg, being this effect related to increased root superoxide dismutase activity, and shoot catalase and ascorbate peroxidase activities. In conclusion, the presence of Zn in the substrate caused a significant reduction in the oxidative stress induced by Hg.

Kinetin improves photosynthetic and antioxidant responses of Nigella sativa to counteract salt stress

The present study involves analysis of growth, photosynthesis, oxidant (H2O2) accumulation, and antioxidant enzyme activities in Nigella sativa L. as affected by foliar kinetin (KIN) application during salt stress. The test plants were treated with 75 or 150 mM NaCl since germination and sprayed with either water or 10 μM KIN in 25 days after emergence. Salt stress, especially at the higher NaCl concentration, was found to induce a substantial decrease in leaf relative water content and subsequently in leaf area and stomatal conductance; chlorophyll content and δ-aminolevulinic acid dehydratase (ALA-D) activity were also affected, resulting in the lower net photosynthetic rate and dry matter production. Moreover, H2O2 content increased in the salt-treated plants, concomitant with an increase in superoxide dismutase and peroxidase activities; however, the activity of catalase declined. Meanwhile KIN was found to reduce appreciably the adverse effects of salinity, besides favorably modulating antioxidant enzyme activities and alleviating oxidative stress in the test plants, to result in a higher yield as compared to the untreated stressed plants. Overall, the results indicate an optimization of antioxidant defense mechanisms and physiological processes by KIN and a significant role of exogenous phytohormones in conferring salt tolerance.

Oral Lead Bullet Fragment Exposure in Northern Bobwhite (Colinus virginianus)

Lead (Pb) is a worldwide environmental contaminant known to adversely affect multiple organ systems in both mammalian and avian species. In birds, a common route of exposure is via oral ingestion of lead particles. Data are currently lacking for the retention and clearance of Pb bullet fragments in gastrointestinal (GI) tract of birds while linking toxicity with blood Pb levels. In the present study, northern bobwhite quail fed a seed-based diet were orally gavaged with Pb bullet fragments (zero, one or five fragments/bird) and evaluated for rate of fragment clearance, and changes in peripheral blood, renal, immune, and gastrointestinal parameters. Based on radiographs, the majority of the birds cleared or absorbed the fragments by seven days, with the exception of one five-fragment bird which took between 7 and 14 days. Blood Pb levels were higher in males than females, which may be related to egg production in females. In males but not females, feed consumption, body weight gain, packed cell volume (PCV), plasma protein concentration, and δ-aminolevulinic acid dehydratase (δ-ALAD) activity were all adversely affected by five Pb fragments. Birds of both sexes that received a single Pb fragment displayed depressed δ-ALAD, suggesting altered hematologic function, while all birds dosed with five bullet fragments exhibited greater morbidity.

S-Allyl-Cysteines Reduce Amelioration of Aluminum Induced Toxicity in Rats

Problem statement: Aluminum (Al) is a trivalent cation found in its ionic form in most kinds of animal tissues and in natural waters everywhere. Approach: It is a potent neurotoxin and has been associated in the pathogenesis of several clinical disorders including Alzheimer’s disease. Results: The aim of the study was to demonstrate the protective effect of S-Allyl-Cysteines (SAC) against Al-induced toxicity in rat model on certain biochemical parameters, lipid peroxidation and oxidative stress enzymes of white albino rats. Six rats per group were divided into various treatment groups. Group one rats were given normal saline and served as control group. Group two animals received Al as aluminum nitrate 32.5 mg (i.p.) for the induction of toxicity. Group three to five received different doses of SAC (25, 50 and 100 mg kg-1) for 3 days after 24 h of Al toxicity. Rats were orally administered their respective doses every day for 3 days. Evaluations were made in blood and tissues. The activity of Acetylcholinesterase (AchE) was inhibited in all the parts of brain after Al intoxication. Significant rise were observed the Activities of Serum Transaminases (AST and ALT) after toxicant exposure. The activity of δ-Aminolevulinic acid Dehydratase (ALAD) in blood and δ-Aminolevulinic Acid Synthetase (ALAS) in brain was decreased after Al exposure. Al significant increased cholesterol, triglyceride, creatinine and urea level in serum. TBARS level was significantly higher and GSH content were significantly lower during toxicity. Total and esterified cholesterol in liver, kidney and brain were increased after Al exposure. Histopathological changes in liver, kidney and brain were also recouped with the therapy. Conclusion/Recommendations: Our data proved that SAC which is a bioactive and bioavailable component of garlic has organosulfur compounds which regulates the thiol status of the cell and scavenges free radicals and work as an antioxidant. Thus SAC effectively reduces cognitive dysfunction and oxidative damage induced by Al.

Biomonitoring of a population of Portuguese workers exposed to lead

Lead is a heavy metal that has been used for many centuries and it is still used for various industrial purposes thanks to its physical and chemical characteristics. Human exposure to lead can result in a wide range of biological effects depending upon the level and duration of exposure. Despite the fact that lead has been found capable of eliciting genotoxic responses in a wide range of tests, not all studies have been conclusive. Although several experimental studies have shown that lead may modulate immune responses, data in exposed humans are still preliminary. The purpose of our study was to evaluate the genotoxic and immunotoxic effects of lead exposure in a group of 70 male workers from two Portuguese factories. The control group comprised 38 healthy males. The exposed individuals showed significantly higher levels of lead in blood and zinc protoporphyrin, and significantly lower δ-aminolevulinic acid dehydratase activity than the controls, suggesting a relatively high lead exposure. Nevertheless, the limit of 70 μg/dl for lead in blood established by the Portuguese regulation was never reached. Results of the comet assay were not modified by the exposure, but a significant increase in the mutation frequency in the exposed workers was obtained in the T-cell receptor mutation assay. Furthermore, data obtained in the analysis of the different lymphocyte subsets showed a significant decrease in %CD8 + cells and a significant increase in the %CD4 +/%CD8 + ratio in exposed individuals with regard to the controls. No clear effect was observed for vitamin D receptor genetic polymorphism on the parameters evaluated. In view of our results showing mutagenic and immunotoxic effects related to lead exposure in occupational settings, it seems that the Portuguese biological exposure limit for lead needs to be revised in order to increase the safety of exposed workers.

Environmental lead exposure as a risk for childhood aplastic anemia

Concern about environmental lead exposure as a significant public health threat has increased as evidence has accumulated regarding adverse health effects at successively lower levels. Aplastic anemia is a hematological disorder of unknown etiology with a high lethality rate. Lead is a known toxicant for the hematopoietic system. Oxidative stress appears to be the possible mode of lead toxicity. We evaluated the effects of blood lead level on oxidative stress parameters in children suffering from aplastic anemia disease. Seventeen children with aplastic anemia disease (15 male and 2 female, age 3-12 y) were recruited in the study group. Fifty one healthy children (45 male and 6 female, age 3-12 y) having normal blood profiles and not suffering from any chronic disease(s) were used as controls. Blood lead level and oxidative stress parameters were determined. Mean blood lead level was significantly higher while δ-aminolevulinic acid dehydratase (δ-ALAD) activity, a biomarker for lead exposure was significantly lower in the study group as compared to the control group (p < 0.05 for each). Thiobarbituric acid reactive species (TBARS), a marker of lipid peroxidation, was significantly higher while the antioxidant glutathione (GSH) level was significantly lower in the study group as compared to the control group (p < 0.05 for each). Activity of the antioxidant enzyme catalase (CAT) was significantly higher in the study group than in the control group (p < 0.05). There was a significant negative correlation of blood lead levels with δ-ALAD (r = -0.45; p < 0.05) and GSH (r = -0.32; p < 0.05), and a positive correlation with TBARS (r = 0.41; p < 0.05) and CAT (r = 0.37; p < 0.05). Although a causal pathway cannot be determined from this study, our results indicated that lead induces oxidative stress in children suffering from aplastic anemia. Lead-induced oxidative stress as an underlying mechanism for aplastic anemia warrants further research.