Delta-aminolevulinic Acid Dehydratase Research Articles

Association between Blood Lead Levels and Delta-Aminolevulinic Acid Dehydratase in Pregnant Women.

Blood lead levels (BLLs) and delta-aminolevulinic acid dehydratase (ALAD) activity are considered biomarkers of lead exposure and lead toxicity, respectively. The present study was designed to investigate the association between BLLs and ALAD activity in pregnant women from Durango, Mexico. A total of 633 pregnant women aged 13–43 years participated in this study. Blood lead was measured by a graphite furnace atomic absorption spectrometer. ALAD activity was measured spectrophotometrically. Mean blood lead was 2.09 ± 2.34 µg/dL; and 26 women (4.1%) crossed the Centers for Disease Control (CDC) recommended level of 5 µg/dL. ALAD activity was significantly lower in women with levels of lead ≥5 µg/dL compared to those with BLLs < 5 µg/dL (p = 0.002). To reduce the influence of extreme values on the statistical analysis, BLLs were analyzed by quartiles. A significant negative correlation between blood lead and ALAD activity was observed in the fourth quartile of BLLs (r = −0.113; p < 0.01). Among women with blood lead concentrations ≥2.2 µg/dL ALAD activity was negatively correlated with BLLs (r = −0.413; p < 0.01). Multiple linear regression demonstrated that inhibition of ALAD in pregnant women may occur at levels of lead in blood above 2.2 µg/dL.

The positive roles of exogenous putrescine on chlorophyll metabolism and xanthophyll cycle in salt-stressed cucumber seedlings

The effects of foliar spray of putrescine (Put; 8 mM) on chlorophyll (Chl) metabolism and xanthophyll cycle in cucumber seedlings were investigated under saline conditions of 75 mM NaCl. Exogenous Put promoted the conversion of uroporhyrinogen III to protoporphyrin IX and alleviated decreases in Chl contents and in a size of the xanthophyll cycle pool under salt stress. Moreover, the Put treatment reduced the activities of uroporphyrinogen III synthase, chlorophyllase, and Mg-dechelatase and downregulated the transcriptional levels of glutamyl-tRNA reductase, 5-aminolevulinate dehydratase, uroporphyrinogen III synthase, uroporphyrinogen III decarboxylase, and chlorophyllide a oxygenase, but significantly increased the expression levels of non-yellow coloring 1-like, pheide a oxygenase, red chlorophyll catabolite reductase, and violaxanthin de-epoxidase. Taken together, these results suggest that Put might improve Chl metabolism and xanthophyll cycle by regulating enzyme activities and mRNA transcription levels in a way that improved the salt tolerance of cucumber plants.

Association of Delta-Aminolevulinic Acid Dehydratase Polymorphism with Blood Lead and Hemoglobin Level in Lead Exposed Workers

Association of Delta-Aminolevulinic Acid Dehydratase Polymorphism with Blood Lead and Hemoglobin Level in Lead Exposed Workers

Pengaruh suplementasi seng dan vitamin B6 terhadap kadar hemoglobin, hematokrit dan indeks eritrosit pasien malaria vivax yang anemia

Background: Zinc supplementation decrease the risk of malaria parasitaemia, increasing ferritin serum level and hemoglobin in patients with malaria. Zinc influence the activity of aminolevulinic acid dehydratase (ALAD) an enzymes that catalizes heme synthesize. Vitamin B6 in pyridoxal 5-phosphate (PLP) from has a role in alpha-aminolevulinic acid (ALA) formation, which is the precursor of heme in hemoglobin. PLP also inhibit the growth of the malaria parasite.Objective: The objective was to analyze the effect of zinc and vitamin B6 supplementation on hemoglobin level, hematocrit and erythrocyte indexs (MCV, MCH and MCHC) of anemic Plasmodium vivax malaria patients.Methods: Double Blind Randomised Controlled Trial with pre and post test design. 30 subjects were divided into two groups: the suplementation group were given zinc 1x10 mg/day with vitamin B6 1x5 mg/day and the control group were given a placebo for 30 days. Data analysis by paired t-test, independent t-test and Mann Whitney.Results: There was an increase in Hb levels in the suplementation group (p=0.0001), the control group (p=0.001) and there was a significant difference on the increase between the two groups (p=0.020). Hematocrit significant increase only in the suplementation group (p=0.0001). There were no differences on erythrocyte index parameter in both groups.Conclusion: Zinc and vitamin B6 supplementation of for 30 days increase the hemoglobin level, hematocrit and there were no effect on erythrocyte indexs of anemic Plasmodium vivax malaria patients.

Ground Squirrel Shooting and Potential Lead Exposure in Breeding Avian Scavengers.

Recreational ground squirrel shooting is a popular activity throughout the western United States and serves as a tool for managing ground squirrel populations in agricultural regions. Belding’s ground squirrels (Spermophilus beldingi) are routinely shot in California, Nevada, and Oregon across habitats that overlap with breeding avian scavengers. Ground squirrels shot with lead (Pb)-based bullets may pose a risk to avian scavengers if they consume carcasses containing Pb fragments. To assess the potential risk to breeding avian scavengers we developed a model to estimate the number, mass, and distribution of Pb fragments in shot ground squirrels using radiographic images. Eighty percent of shot carcasses contained detectible Pb fragments with an average of 38.6 mg of Pb fragments. Seven percent of all carcasses contained Pb fragment masses exceeding a lethal dose for a model raptor nestling (e.g. American kestrel Falco sparverius). Bullet type did not influence the number of fragments in shot ground squirrels, but did influence the mass of fragments retained. Belding’s ground squirrels shot with .17 Super Mag and unknown ammunition types contained over 28 and 17 times more mass of Pb fragments than those shot with .22 solid and .22 hollow point bullets, respectively. Ground squirrel body mass was positively correlated with both the number and mass of Pb fragments in carcasses, increasing on average by 76% and 56% respectively across the range of carcass masses. Although the mass of Pb retained in ground squirrel carcasses was small relative to the original bullet mass, avian scavenger nestlings that frequently consume shot ground squirrels may be at risk for Pb-induced effects (e.g., physiology, growth, or survival). Using modeling efforts we found that if nestling golden eagles (Aquila chrysaetos), red-tailed hawks (Buteo jamaicensis), and Swainson’s hawks (B. swainsoni) consumed shot ground squirrels proportionately to the nestling’s mass, energy needs, and diet, 100% of the nestling period would exceed a 50% reduction in delta-aminolevulinic acid dehydratase production threshold, the last 13–27% of the nestling stage would exceed a reduced growth rate threshold, but no nestlings would be expected to exceed a level of Pb ingestion that would be lethal.

Hepatic porphyria: A narrative review.

Porphyrias are a group of metabolic disorders, which result from a specific abnormality in one of the eight enzymes of the heme biosynthetic pathway. These have been subdivided based on the predominant site of enzyme defect into hepatic and erythropoietic types and based on clinical presentation into acute neurovisceral and cutaneous blistering porphyrias. This review focuses on hepatic porphyrias, which include acute intermittent porphyria (AIP), variegate porphyria (VP), hereditary coproporphyria (HCP), aminolevulinic acid dehydratase deficiency porphyria (ADP), and porphyria cutanea tarda (PCT). Of these, AIP and ADP are classified as acute porphyria, PCT as cutaneous, while VP and HCP present with both acute and cutaneous clinical manifestations. Porphobilinogen levels in a spot urine sample is the initial screening test for the diagnosis of acute hepatic porphyria, and plasma with spot urine porphyrin levels is the initial screening test to approach patients suspected of cutaneous porphyria. Specific biochemical porphyrin profile for each porphyria helps in determining the specific diagnosis. Pain relief and elimination of triggering agents are the initial steps in managing a patient presenting with an acute attack. Intravenous glucose administration terminates the mild episode of acute porphyria, with intravenous hemin needed for management of moderate to severe episodes. Liver transplantation is curative and may be needed for patients with a life-threatening acute porphyria attack or for patients with recurrent acute attacks refractory to prophylactic treatment. Of the cutaneous porphyrias, PCT is the most common and is frequently associated with a combination of multiple susceptibility factors such as alcohol use, smoking, hepatitis C virus infection, HIV infection, estrogen use, and mutations of the hemochromatosis gene. Regular phlebotomy schedule and low-dose hydroxychloroquine are effective and safe treatment options for management of PCT.

Effects of gallic acid on delta - aminolevulinic dehydratase activity and in the biochemical, histological and oxidative stress parameters in the liver and kidney of diabetic rats.

Diabetes mellitus (DM) is characterised by hyperglycaemia associated with the increase of oxidative stress. Gallic acid has potent antioxidant properties. The aim of this study was to evaluate the effect of gallic acid on the biochemical, histological and oxidative stress parameters in the liver and kidney of diabetic rats. Male rats were divided in groups: control, gallic acid, diabetic and diabetic plus gallic acid. DM was induced in the animals by intraperitoneal injection of streptozotocin (65mg/kg). Gallic acid (30mg/kg) was administered orally for 21days. Our results showed an increase in reactive species levels and lipid peroxidation, and a decrease in activity of the enzymes superoxide dismutase and delta-aminolevulinic acid dehydratase in the liver and kidney of the diabetic animals (P<0.05). Gallic acid treatment showed protective effects in these parameters evaluated, and also prevented a decrease in the activity of catalase and glutathione S-transferase, and vitamin C levels in the liver of diabetic rats. In addition, gallic acid reduced the number of nuclei and increased the area of the core in hepatic tissue, and increased the glomerular area in renal tissue. These results indicate that gallic acid can protect against oxidative stress-induced damage in the diabetic state.

The Remarkable Character of Porphobilinogen Synthase.

Porphobilinogen synthase (PBGS), also known as 5-aminolevulinate dehydratase, is an essential enzyme in the biosynthesis of all tetrapyrroles, which function in respiration, photosynthesis, and methanogenesis. Throughout evolution, PBGS adapted to a diversity of cellular niches and evolved to use an unusual variety of metal ions both for catalytic function and to control protein multimerization. With regard to the active site, some PBGSs require Zn2+; a subset of those, including human PBGS, contain a constellation of cysteine residues that acts as a sink for the environmental toxin Pb2+. PBGSs that do not require the soft metal ion Zn2+ at the active site instead are suspected of using the hard metal Mg2+. The most unexpected property of the PBGS family of enzymes is a dissociative allosteric mechanism that utilizes an equilibrium of architecturally and functionally distinct protein assemblies. The high-activity assembly is an octamer in which intersubunit interactions modulate active-site lid motion. This octamer can dissociate to dimer, the dimer can undergo a hinge twist, and the twisted dimer can assemble to a low-activity hexamer. The hexamer does not have the intersubunit interactions required to stabilize a closed conformation of the active site lid. PBGS active site chemistry benefits from a closed lid because porphobilinogen biosynthesis includes Schiff base formation, which requires deprotonated lysine amino groups. N-terminal and C-terminal sequence extensions dictate whether a specific species of PBGS can sample the hexameric assembly. The bulk of species (nearly all except animals and yeasts) use Mg2+ as an allosteric activator. Mg2+ functions allosterically by binding to an intersubunit interface that is present in the octamer but absent in the hexamer. This conformational selection allosteric mechanism is purported to be essential to avoid the untimely accumulation of phototoxic chlorophyll precursors in plants. For those PBGSs that do not use the allosteric Mg2+, there is a spatially equivalent arginine-derived guanidium group. Deprotonation of this residue promotes formation of the hexamer and accounts for the basic arm of the bell-shaped pH vs activity profile of human PBGS. A human inborn error of metabolism known as ALAD porphyria is attributed to PBGS variants that favor the hexameric assembly. The existence of one such variant, F12L, which dramatically stabilizes the human PBGS hexamer, allowed crystal structure determination for the hexamer. Without this crystal structure and octameric PBGS structures containing the allosteric Mg2+, it would have been difficult to decipher the structural basis for PBGS allostery. The requirement for multimer dissociation as an intermediate step in PBGS allostery was established by monitoring subunit disproportionation during the turnover-dependent transition of heteromeric PBGS (comprised of human wild type and F12L) from hexamer to octamer. One outcome of these studies was the definition of the dissociative morpheein model of protein allostery. The phylogenetically variable time scales for PBGS multimer interconversion result in atypical kinetic and biophysical behaviors. These behaviors can serve to identify other proteins that use the morpheein model of protein allostery.

Protective effect of Allium sativum (garlic) aqueous extract against lead-induced oxidative stress in the rat brain, liver, and kidney.

The present investigation was undertaken to evaluate the ameliorative activity of Allium sativum against lead-induced oxidative stress in the brain, liver, and kidney of male rats. Four groups of male Wistar strain rats (100-120g) were taken: group 1 received 1000mg/L sodium acetate and group 2 was given 1000mg/L lead acetate through drinking water for 2weeks. Group 3 and 4 were treated with 250mg/kg body weight/day of A. sativum and 500mg/kg body weight/day of A. sativum, respectively, by oral intubation for a period of 2weeks along with lead acetate. The rats were sacrificed after treatment and the brain, liver, and kidney were isolated on ice. In the brain, four important regions namely the hippocampus, cerebellum, cerebral cortex, and brain stem were separated and used for the present investigation. Blood was also drawn by cardiac puncture and preserved in heparinized vials at 4°C for estimation of delta-aminolevulinic acid dehydratase (ALAD) activity. The results showed a significant (p<0.05) increase in reactive oxygen species (ROS), lipid peroxidation products (LPP), total protein carbonyl content (TPCC), and lead in the selected brain regions, liver, and kidney of lead-exposed group compared with their respective controls. Blood delta-ALAD activity showed a significant (p<0.05) decrease in the lead-exposed rats. However, the concomitant administration of A. sativum resulted in tissue-specific recovery of oxidative stress parameters namely ROS, LPP, and TPCC. A. sativum treatment also restored the blood delta-ALAD activity back to control. Overall, our results indicate that A. sativum administration could be an effective antioxidant treatment strategy for lead-induced oxidative insult.

Porphyria: Analysis of Register from Brazilian Association of Porphyria (ABRAPO)

1.1.Background:The porphyria is a group of rare metabolic disorders that arise from deficiencies in the heme biosynthetic pathway. The prevalence in Europe is 1-2:100,000 inhabitants. These disorders occur mostly due to mutations in the genes encoding enzymes involved in heme production. They are classified and divided into acute (ALA Dehydratase Deficiency [ALADP], Acute Intermittent Porphyria [AIP], Variegate Porphyria [VP], Hereditary Coproporphyria [HCP]), chronic (Congenital Erythropoietic Porphyria [CEP], Erythropoietic Porphyria [EPP], Porphyria Cutanea Tarda [PCT] and Hepato Erythropoietic Porphyria [HEP]). AIP is the most common form of hepatic porphyria and symptoms are often begin after puberty and consist of acute neurovisceral signs, abdominal pain, vomiting, constipation, tachycardia, fever, hypertension and alterations in the central nervous system. 1.2.Aim:To study the porphyria frequency in Brazil by Associacao Brasileira de Porfiria (ABRAPO- Brazilian Porphyria Association). 1.3.Methods:We study the frequency of porphyria in 439 cases of patients with porphyria diagnosis from ABRAPO from 2007 to 2015 and data were analyzed with Microsoft Excel® program. 1.4.Results:We analyzed 439 cases consisting of 74.2% female. 59% percent had been diagnosed with AIP, 22% PCT, 4% HCP, 4% EPP, 2.5% VP, 1.1% CEP, 0.9% HEP and 0.4% ALADP. 1.5.Conclusion:Our analysis revealed similar epidemiological characteristics as seen in the United States and United Kingdom. In Brazil, porphyria should be studied more carefully to assess, properly diagnosis and treatment.

The Porphyrias

The porphyrias are uncommon disorders caused by deficiencies in the activities of enzymes of the heme biosynthetic pathway. The enzymatic defects that cause porphyrias are inherited, with the exception of porphyria cutanea tarda, which is primarily acquired. In all porphyrias, there is significant interplay between genetic traits and acquired or environmental factors in the expression of clinical symptoms. This review discusses the classification, pathophysiology, and clinical presentations of the porphyrias. These include those associated with neurovisceral attacks (acute intermittent porphyria, variegate porphyria, hereditary coproporphyria, and δ-aminolevulinic acid dehydratase [alad] deficiency porphyria) and the porphyrias associated with cutaneous photosensitivity (porphyria cutanea tarda, hepatoerythropoietic porphyria, erythropoietic protoporphyria, and congenital erythropoietic porphyria). Specific emphasis on the epidemiology, molecular defects and pathophysiology, clinical features, diagnosis, and treatment are discussed for each of these disorders. A table lists the safe and unsafe drugs for patients with porphyrias. Figures illustrate the genetic pathways of the disorders and the activities of enzymes of the heme biosynthetic pathway. This review contains 2 highly rendered figures, 1 table, and 96 references.

Chronic administration of methionine and/or methionine sulfoxide alters oxidative stress parameters and ALA-D activity in liver and kidney of young rats.

High levels of methionine (Met) and methionine sulfoxide (MetO) are found in several genetic abnormalities. Oxidative stress is involved in the pathophysiology of many inborn errors of metabolism. However, little is known about the role of oxidative damage in hepatic and renal changes in hypermethioninemia. We investigated the effect of chronic treatment with Met and/or MetO on oxidative stress parameters in liver and kidney, as lipid peroxidation (TBARS), total sulfhydryl content (SH), reactive oxygen species (ROS) and enzymes activities superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and delta aminolevulinic dehydratase (ALA-D). Serum biochemical parameters were evaluated. Wistar rats were treated daily with two subcutaneous injections of saline (control), Met (0.2-0.4g/kg), MetO (0.05-0.1g/kg) and the association between these (Met plus MetO) from the 6th to the 28thday of life. Our data demonstrated an increase of glucose and urea levels in all experimental groups. Cholesterol (MetO and Met plus MetO) were decreased and triglycerides (MetO) were increased. SOD (MetO and Met plus MetO) and CAT (Met, MetO and Met plus MetO) activities were decreased, while GPx was enhanced by MetO and Met plus MetO treatment in liver. In kidney, we observed a reduction of SH levels, SOD and CAT activities and an increase of TBARS levels in all experimental groups. ROS levels in kidney were increased in MetO and Met plus MetO groups. ALA-D activity was enhanced in liver (MetO and Met plus MetO) and kidney (Met plus MetO). These findings help to understand the pathophysiology of hepatic and renal alterations present in hypermethioninemia.

Lead-Related Genetic Loci, Cumulative Lead Exposure and Incident Coronary Heart Disease: The Normative Aging Study.

BackgroundCumulative exposure to lead is associated with cardiovascular outcomes. Polymorphisms in the δ-aminolevulinic acid dehydratase (ALAD), hemochromatosis (HFE), heme oxygenase-1 (HMOX1), vitamin D receptor (VDR), glutathione S-transferase (GST) supergene family (GSTP1, GSTT1, GSTM1), apolipoprotein E (APOE),angiotensin II receptor-1 (AGTR1) and angiotensinogen (AGT) genes, are believed to alter toxicokinetics and/or toxicodynamics of lead.ObjectivesWe assessed possible effect modification by genetic polymorphisms in ALAD, HFE, HMOX1, VDR, GSTP1, GSTT1, GSTM1, APOE, AGTR1 and AGT individually and as the genetic risk score (GRS) on the association between cumulative lead exposure and incident coronary heart disease (CHD) events.MethodsWe used K-shell-X-ray fluorescence to measure bone lead levels. GRS was calculated on the basis of 22 lead-related loci. We constructed Cox proportional hazard models to compute adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for incident CHD. We applied inverse probability weighting to account for potential selection bias due to recruitment into the bone lead sub-study.ResultsSignificant effect modification was found by VDR, HMOX1, GSTP1, APOE, and AGT genetic polymorphisms when evaluated individually. Further, the bone lead-CHD associations became larger as GRS increases. After adjusting for potential confounders, a HR of CHD was 2.27 (95%CI: 1.50–3.42) with 2-fold increase in patella lead levels, among participants in the top tertile of GRS. We also detected an increasing trend in HRs across tertiles of GRS (p-trend = 0.0063).ConclusionsOur findings suggest that lead-related loci as a whole may play an important role in susceptibility to lead-related CHD risk. These findings need to be validated in a separate cohort containing bone lead, lead-related genetic loci and incident CHD data.

Lead-Related Genetic Loci, Cumulative Lead Exposure and Incident Coronary Heart Disease: The Normative Aging Study

Introduction: Cumulative exposure to lead is associated with cardiovascular outcomes. Polymorphisms in the aminolevulinic acid dehydratase (ALAD), hemochromatosis (HFE), heme oxygenase-1 (HMOX-1), vitamin D receptor (VDR), glutathione S-transferase (GST) supergene family (GSTP-1, GSTT-1, GSTM-1), apolipoprotein E (APOE) and angiotensinogen (AGT) genes, are believed to alter toxicokinetics and/or toxicodynamics of lead. We assessed possible effect modification by genetic polymorphisms in ALAD, HFE, HMOX-1, VDR, GSTP-1, GSTT-1, GSTM-1, APOE, AGTR-1 and AGT individually and as the genetic risk score (GRS) on the association between cumulative lead exposure and incident coronary heart disease (CHD) events. Methods: We used K-shell-X-ray fluorescence to measure bone lead levels. GRS was calculated on the basis of 22 lead-related loci. We constructed Cox proportional hazard models to compute adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for incident CHD. We applied inverse probability weightin...

Blood pressure and occupational exposure to noise and lead (Pb): A cross-sectional study.

Several studies have explored the hypothesis that low blood lead (PbB) and high noise levels may be associated with an increased risk of hypertension. To assess the possible relationship between occupational exposure to lead (Pb) and noise and elevated blood pressure, we studied 105 workers (age: 41.27 ± 6.25 years and length of employment: 4.12 ± 5.33 years) employed in a Pb battery recycling plant by measuring A-weighted equivalent sound level, PbB, δ-aminolevulinic acid dehydratase (ALAD) activity and zinc protoporphyrin (ZPP) levels and systolic and diastolic blood pressure (SBP and DBP). Results showed that occupational exposure to higher ambient Pb and noise levels was related to slightly increased SBP and DBP. PbB values correlated significantly with SBP and DBP, whereas noise levels correlated neither with SBP nor with DBP. Furthermore, workers exposed to higher ambient Pb had higher PbB and ZPP and showed more decreased ALAD activity. Blood pressure does not correlate with noise exposure but only with PbB concentration.

Doss Porphyria (δ-Aminolevulinic Acid Dehydratase Porphyria) Presenting with Acute Onset Flaccid Paralysis

δ–Aminolevulinic acid dehydratase porphyria is an autosomal recessive disorder of heme synthesis resulting from deficiency of δ-aminolevulinic acid dehydratase (ALAD). Patients present with fatal neurovisceral manifestations and motor neuropathy. Here we report a patient with rapidly progressive flaccid tetraplegia with respiratory and bulbar paralysis. The importance of early diagnosis, prompt treatment and screening of relatives is stressed.J Nepal Paediatr Soc 2015;35(3):280-282

Nanocurcumin Prevents Oxidative Stress Induced following Arsenic and Fluoride Co-exposure in Rats

&lt;p&gt;The present study is in continuation of our previous efforts to investigate the preventive efficacy of encapsulated curcumin nanoparticles (nanocurcumin) in mitigating effects of arsenic and/or fluoride. Curcumin was encapsulated in chitosan nanoparticles having a size distribution in the range of 50 nm. Sodium arsenite (2 mg/kg, orally) and Fluoride (50 ppm in drinking water) either alone or in combination were administered to male Wistar rats for four weeks to evaluate the efficacy of nanocurcumin (15 mg/kg) in rats. The preventive efficacy of nanocurcumin was evaluated against various altered biochemical variables suggestive of oxidative stress in liver and kidneys, and concentration of As and F in blood. Nanocurcumin co-administration with arsenic and fluoride resulted in lowering of reactive oxygen species and restoration of blood glutathione level which were found to be altered in arsenic and fluoride intoxicated groups. Nanocurcumin were also found to be effective in reversing δ-aminolevulinic acid dehydratase (ALAD) inhibition caused by arsenic exposure. The most promising result from our study shows that nanocurcumin removes not only arsenic but also fluoride from blood which may be due to the enhanced bioavailability and moderate chelating potential of nanocurcumin.&lt;/p&gt;

Effects of zinc against mercury toxicity in female rats 12 and 48 hours after HgCl2 exposure.

This work investigated the toxicity of inorganic mercury and zinc preventive effects in female rats sacrificed 12 or 48 h after HgCl2 exposure. Female Wistar rats were subcutaneously injected with ZnCl2 (27 mg/kg) or saline (0.9 %), and 24 h later they were exposed to HgCl2 (5 mg/kg) or saline (0.9 %). Rats sacrificed 12 hours after Hg administration presented an increase in kidney weight and a decrease in renal ascorbic acid levels. Zinc pretreatment prevented the renal weight increase. Rats sacrificed 48 h after Hg exposure presented a decrease in body weight gain, an increase in renal weight, a decrease in renal δ-aminolevulinic acid dehydratase activity, an increase in serum creatinine and urea levels, and a decrease in kidney total thiol levels. Zinc pretreatment partly prevented the decrease in body weight gain and increase in creatinine levels, in addition to totally preventing renal δ-aminolevulinic acid dehydratase inhibition. Mercury accumulation in the kidney and liver in both periods was observed after Hg administration. These results show the different Hg effects along the time of intoxication, and a considerably preventive effect of zinc against Hg toxicity.

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.

Lead exposure reduces carotenoid-based coloration and constitutive immunity in wild mallards.

The ingestion of spent lead (Pb) from ammunition is a known cause of mortality in waterfowl, but little is known about sublethal effects produced by Pb poisoning on birds, especially in wild populations. The authors studied potential sublethal effects associated with Pb exposure in mallards (Anas platyrhynchos) from the Ebro delta (northeastern Spain) after a ban on Pb ammunition. They analyzed the relationships between blood Pb levels and oxidative stress, immune response, and carotenoid-based coloration, which are known to be influenced by oxidative stress. Levels of Pb were reduced by half from 6 yr to 9 yr after the ban. Lipid peroxidation was positively related to Pb levels in females. The δ-aminolevulinic acid dehydratase activity was suppressed by Pb exposure and negatively associated with the activity of antioxidant enzymes. Carotenoid levels were positively associated with blood Pb concentration in both sexes, and males with higher Pb levels presented a less intense coloration in legs and beak. Levels of Pb were positively related to hemolytic activity of circulating immune system components and negatively related to lysozyme levels. In summary, Pb exposure was associated in a gender-specific way with increased oxidative stress, consequences on color expression, and impaired constitutive immunity. In females, antioxidants seemed to be allocated mostly in reproduction rather than in self-maintenance, whereas males seemed to better maintain oxidative balance to the detriment of coloration. Environ Toxicol Chem 2016;35:1516-1525. © 2015 SETAC.