And Δ-aminolevulinic Acid Dehydratase Research Articles

Redox status upon herbicides application in the control of Lolium multiflorum (2n and 4n) as weed

Lolium multiflorum Lam. is a winter weed of difficult control found as diploid (2n) and tetraploid plants (4n). Our study aimed to evaluate the responses of antioxidant enzymes and lipid peroxidation, in both diploid and tetraploid ryegrass varieties. Treatments consisted of control plants (without any herbicide application), and four herbicides with different mechanisms of action. Leaf material was collected 36 h after treatment imposition to determine the lipid peroxidation by ferrous oxidation-xylenol (FOX) content, and the activity of the enzymes superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), guaiacol peroxidase (GPX), glutathione-S-transferase (GST), and δ-aminolevulinic acid dehydratase (ALAD). Both ryegrass varieties showed oxidative stress mainly due to a downregulated decreased (>31%) in SOD activity and an increase (>32%) in lipid peroxidation (FOX), mainly in ryegrass genotypes exposed to haloxyfop, glyphosate, and iodosulfuron. On the other hand, clethodim-treated plants had an increase in SOD and APX activities, associated with a reduced ALAD activity in both 2n (32%) and 4n (11%) genotypes. In general, the 2n genotype was more affected than the 4n genotype.

Relationship Between Lead (Pb) Concentration in Soil, Grass , Blood, Milk and δ-aminolevulinic Acid Dehydratase (ALAD) Activity , Hemoglobin (Hb) and Hematocrit (Hct) in Grazing Cows from Vicinity of Smelter “Trepça” in Kosovo

Relationship Between Lead (Pb) Concentration in Soil, Grass , Blood, Milk and δ-aminolevulinic Acid Dehydratase (ALAD) Activity , Hemoglobin (Hb) and Hematocrit (Hct) in Grazing Cows from Vicinity of Smelter “Trepça” in Kosovo

Effect of lead exposure and nutritional iron-deficiency on immune response: A vaccine challenge study in rats

The prevalence of iron (Fe) deficiency and subclinical lead (Pb) toxicity is high in developing countries like India, and information on their potential additive effects on immune responses is scant. The current study assessed immune parameters in dual Pb-exposed\\Fe-deficient weanling SD rats. Rats were fed a control (CD) or Fe-deficient (ID) diet for 4 weeks and then evaluated for hemoglobin (Hb) and serum Fe status. Then, half the rats in each group began to receive daily oral Pb exposure (25 mg/4 ml/kg BW; gavage) or vehicle for a further 4 weeks (while maintained on original respective diets). After the 4-weeks of dosing, rats were assessed for Hb and serum Fe, and for blood lead level (BLL) and δ-aminolevulinic acid dehydratase (ALAD) activity. At this point, half the rats in each group (now n = 8) were then vaccinated with tetanus toxoid (TT), and then two boosters at 2-week intervals. All the time, rats stayed on their original respective diets along with exposure to Pb on alternate days. At 2 weeks after the final booster, rats were euthanized and blood collected to assess total/specific IgG and IgM levels; mucosal (intestinal) IgA levels were also determined. Spleens were taken to assess CD4+ and CD8+ cell levels and for ex vivo measures of splenocyte proliferation/TH1 and TH2 cytokine formation. The results indicated significant lowering of Hb and serum Fe levels in ID rats and increased blood Pb and decreased ALAD activity in all Pb-exposed rats. Fe-deficiency alone induced significant increases in ALAD activity, but only in an absence of Pb. While there was no impact of any regimen on total or TT-specific IgG, significant decreases in mucosal IgA and TT-specific IgM were seen in ID-fed Pb-exposed rats. CD4+ cell levels were not impacted by treatment; CD8+ levels were increased in all ID/Pb-exposed rats. Ex-vivo splenocyte proliferation was significantly higher among vaccinated rats, as well as ID-fed Pb-exposed unvaccinated rats. Cytokine formation in all cases was highly variable. The results suggest that Fe deficiency compromised cell-mediated, mucosal, and/or humoral immune response-related endpoints and that Pb exposure during the deficiency further impacted these outcomes.

Acute hepatic porphyrias: Identification of 46 hydroxymethylbilane synthase, 11 coproporphyrinogen oxidase, and 20 protoporphyrinogen oxidase novel mutations

The acute hepatic porphyrias (AHPs) are inborn errors of heme biosynthesis, which include three autosomal dominant porphyrias, Acute Intermittent Porphyria (AIP), Hereditary Coproporphyria (HCP), and Variegate Porphyria (VP), and the ultra-rare autosomal recessive porphyria, δ-Aminolevulinic Acid Dehydratase Deficiency Porphyria (ADP). AIP, HCP, VP, and ADP each results from loss-of-function (LOF) mutations in their disease-causing genes: hydroxymethylbilane synthase (HMBS); coproporphyrinogen oxidase (CPOX); protoporphyrinogen oxidase (PPOX), and δ-aminolevulinic acid dehydratase (ALAD), respectively. During the 11-year period from January 1, 2007 through December 31, 2017, the Mount Sinai Porphyrias Diagnostic Laboratory diagnosed 315 unrelated AIP individuals with HMBS mutations, including 46 previously unreported mutations, 29 unrelated HCP individuals with CPOX mutations, including 11 previously unreported mutations, and 54 unrelated VP individuals with PPOX mutations, including 20 previously unreported mutations.Overall, of the 1692 unrelated individuals referred for AHP molecular diagnostic testing, 398 (23.5%) had an AHP mutation. Of the 650 family members of mutation-positive individuals tested for an autosomal dominant AHP, 304 (46.8%) had their respective family mutation. These data expand the molecular genetic heterogeneity of the AHPs and document the usefulness of molecular testing to confirm the positive biochemical findings in symptomatic patients and identify at-risk asymptomatic family members.

Oxidative stress in opium users after using lead-adulterated opium: The role of genetic polymorphism

Use of lead-adulterated opium has become one of the major sources of lead poisoning in Iran. This study was designed to assess clinical effects and oxidative stress and its association with GSTM1, GSTT1, NQO1, and ALAD genes polymorphisms and blood lead level (BLL) in lead-adulterated opium users. The oxidative stress status in 192 opium users with lead poisoning symptoms measured and compared with 102 healthy individuals. Gluthatione S-transferase (GST)-M1 and -T1 genes deletion, NQO1 rs1800566, and δ-aminolevulinic acid dehydratase (ALAD) rs1800435 polymorphisms were determined using PCR and PCR-RFLP. The relation between the polymorphisms, BLL, and oxidative stress parameters were analysed using multivariate linear regressions. The common symptoms of lead toxicity were gastrointestinal and neurologic complications. Oxidative stress was significantly higher in opium addicts and lipid peroxidation significantly correlated with BLL. There was significant association between ALAD rs1800435 and BLL, and the BLL was significantly lower in the patients with ALAD 1-2 genotype. Use of lead-adulterated opium causes high frequency of lead toxicity symptoms, hematological and biochemical abnormalities, and oxidative stress which are associated with BLL. Route of opioid use and the polymorphism of rs1800435 in ALAD gene are the major determinants of BLL in lead-adulterated opium users.

Spatial and seasonal biomarker responses in the clam Ruditapes decussatus

The clam Ruditapes decussatus is an important resource to preserve in coastal lagoon systems around the Mediterranean including the South Portugal. To assess spatial and temporal biomarker responses to contamination in the species, a multibiomarker approach was conducted using antioxidant enzymes, MFO system phase I and II; acetylcholinesterase, metallothionein (MT), δ-aminolevulinic acid dehydratase and lipid peroxidation (LPO). The condition index (CI), metals and polycyclic aromatic hydrocarbons (PAHs) were also determined. The levels of contaminants were not particularly high and the antioxidant enzymes, acetylcholinesterase (AChE), MT in the digestive gland, and δ-aminolevulinic acid dehydratase (ALAD) do not provide a suitable seasonal and spatial discrimination reversely to that regarding CYP450, glutathione-S-transferase (GST), MT in the gills, and LPO in both tissues. However, even those could vary with natural variables that may act as confounding factors. Thus, seasonal variability and natural range of biomarker responses must be carefully and accurately taken into account in ecotoxicological approaches of environmental quality assessment programmes.

Assessment of Immunotoxicity Parameters in Individuals Occupationally Exposed to Lead

Although adverse health effects produced by lead (Pb) have long been recognized, studies regarding the immunotoxic effects of occupational exposure report conflicting results. In a previous study, alterations in some immunological parameters were noted in 70 Pb-exposed workers. In view of these results, it was of interest to extend this study comprising a larger population and increasing the number of immunological endpoints assessed. Accordingly, in this study the immunotoxic effects of occupational exposure to Pb were assessed by analyzing (1) percentages of lymphocyte subsets (CD3+, CD4+, CD8+, CD19+, and CD56+/16+); (2) concentration of plasma cytokines, namely, interleukin (IL) 2, IL4, IL6, IL10, tumor necrosis factor (TNF) α, and interferon (IFN) γ; and (3) plasma concentrations of neopterin, tryptophan (Trp), and kynurenine (Kyn). In addition, the possible influence of genetic polymorphisms in the vitamin D receptor (VDR) and δ-aminolevulinic acid dehydratase (ALAD) genes on immunotoxicity parameters was studied. Exposed workers showed significant decreases in %CD3+, %CD4+/%CD8+ ratio, IL4, TNFα, IFNγ, and Kyn to Trp ratio (Kyn/Trp), and significant increases in %CD8+, IL10, and Trp levels. All these parameters, except Trp, were significantly correlated with exposure biomarkers. No significant influence of genetic polymorphisms was observed. Significant correlation between Kyn/Trp and neopterin concentrations suggests an involvement of indoleamine 2,3-dioxygenase in the Trp metabolic alterations, which may contribute to some of the immune alterations observed. Results obtained suggest that occupational exposure to PB may influence the immune system by impairing several mechanisms, which might ultimately produce deregulation of the immune response and diminish immunosurveillance in exposed individuals.

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.

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.

Protective effect of Smilax glabra extract against lead-induced oxidative stress in rats

Ethnopharmacological relevance Smilax glabra Roxb. is a traditional Chinese herb, the rhizome of Smilax glabra has been used in folk medicine for the treatment of lead poisoning. Aims of the study The present study was conducted to investigate the protective role of Smilax glabra extract (SGE) individually or combined with meso-2,3-dimercaptosuccinic acid (DMSA) against the effects of lead acetate on oxidative stress and lead burden in rats. Materials and methods The biochemical parameters and enzymes in different treated rats were determined by commercial kits. The metal concentrations were measured using atomic absorption spectrophotometer. Results SGE (300 mg/kg) showed very low toxicity to organs in non-lead exposed rats. Administration of SGE individually had no effect on blood zinc protoporphyrin (ZPP) level but significantly enhanced the glutathione (GSH) content and δ-aminolevulinic acid dehydratase (ALAD), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activities in lead exposed rats. The co-treatment of SGE and DMSA had a synergism in increasing brain, liver and kidney superoxide dismutase (SOD), catalase (CAT) activities and GSH level, and decreasing oxidized glutathione (GSSG) and thiobarbituric acid reactive substances (TBARS) levels. Moreover, the co-treatment could improve the hepatic and renal histopathology changes. SGE as chelating agent showed significant efficiency in reducing blood and tissue lead burden. Conclusions The in vivo results suggested that SGE individually or combined with DMSA exhibited remarkable protective effects on lead-induced oxidative stress and lead burden in rats.

Occupational exposure of farm workers to pesticides: Biochemical parameters and evaluation of genotoxicity

To assess the effects of exposure to complex mixtures of pesticides in farm workers from two communities from Rio Grande do Sul, Brazil, we evaluated the activities of butyrylcholinesterase (BChE) and δ-aminolevulinic acid dehydratase (ALA-D) enzymes, hematological, lipid parameters, and genotoxicity using two tests to detect DNA damage, the Comet assay in peripheral blood leukocytes and the micronucleus (MN) test in oral mucosa cells. The use of personal protective equipment (PPE), age and smoke habits were considered in the analysis. There was a significant decrease in the BChE and ALA-D activities in farm workers ( n = 37) relative to the control group ( n = 20) (P ≤ 0.05 and P ≤ 0.001, respectively). The Comet assay in peripheral blood leukocytes showed that the Damage index and Damage frequency observed in the exposed group were significantly higher in relation to the controls ( P ≤ 0.001, and P ≤ 0.05, respectively). No differences were detected regarding the hematological parameters, lipids profile, and MN frequencies. In addition, no significant differences were observed between younger (≤ 38 years) and older subjects (> 38 years), or between smokers and non-smokers within the groups, either by Comet assay or MN test. However, the use of PPE seems to be important in the prevention of contamination, as suggested by BChE levels and Comet assay results.

Metallothioneins (MTs) and δ-aminolevulinic acid dehydratase (ALAd) as biomarkers of metal pollution in great tits ( Parus major) along a pollution gradient

Biomonitoring allows an integrated evaluation of different aspects of exposure, accumulation and effects to environmental pollution, simultaneously accounting for the natural variety between individuals in an ecosystem. In this study, the effects of increased metal accumulation were evaluated at the biochemical level in terms of two biomarker responses in the great tit ( Parus major), a small insectivorous songbird, along an established metal pollution gradient. Metal concentrations in internal tissues (liver and kidney) and blood indicated that lead and cadmium were the most important metals in the pollution gradient under study. At the biochemical level, induction of metal binding protein metallothionein (MT) in liver and kidney reflected cadmium concentrations in these tissues ( R 2 = 0.42 and R 2 = 0.94 respectively, n = 19), although in kidney, MT induction was not sufficient to complex all cadmium present. Secondly, the activity of the enzyme δ-aminolevulinic acid dehydratase (ALAd) in blood decreased exponentially in response to increased lead accumulation ( R 2 = 0.70, n = 18) and represents therefore a specific effect marker for lead exposure. In the highest polluted area, an ALAd inhibition of 85% was reported. Since a higher metal exposure resulted in an increased metal accumulation and subsequent biomarker responses in a dose-dependent way, this study indicates the applicability of ALAd and MT levels in great tits for biomonitoring responses to heavy metal pollution.

Effect of estradiol on heme biosynthetic pathway in lead-poisoned rabbits

To clarify the effect of the female hormone estradiol (Est) on heme biosynthesis in lead-poisoned rabbits, parameters indicating lead exposure, such as free erythrocyte protoporphyrin (FEP) level and δ-aminolevulinic acid dehydratase (ALA-D) activity, were determined. Twenty-six male Japanese white rabbits (body weight (BW), 3kg) were divided into four groups: I (control), II (Est), III (Pb), IV (Est+Pb). About 3 weeks after castration, Est (3 mg/kg of BW) was injected intramuscularly, and 2 weeks thereafter, lead (1.2 mg/kg of BW) was injected intravenously. After the initial injection of each of these substances, the same dose of each of these substances was injected once a week until the 9th week. In groups III and IV, FEP level increased and ALA-D activity in the erythrocytes, bone marrow and liver decreased with an increase in lead concentration in blood. FEP level decreased significantly (p<0.01) in the 8th and 10th weeks after Est injection in group IV compared to with that in group III and was not elevated in group II compared with that in group I. ALA-D activity in the erythrocytes, bone marrow and liver increased significantly in group II compared with that in group I, whereas Ht and Hb levels decreased in group II compared with those in group I, and decreased in group IV compared with those in group III. The level of iron in plasma (Fe-P) was within the normal range during experiment. In this study, Est did not increase FEP level. From the above results regarding FEP level and ALA-D activity, Est may prevent an increase in FEP level caused by lead. Ht and Hb levels, which are the parameters of anemia, decreased mainly as a result of Est exposure rather than lead exposure.

Meso 2,3-dimercaptosuccinic acid (DMSA) and monoisoamyl DMSA effect on gallium arsenide induced pathological liver injury in rats

The effect of meso 2,3-dimercaptosuccinic acid (DMSA) and monoisoamyl DMSA (MiADMSA) on gallium arsenide (GaAs) induced liver damage was studied. The oral feeding rat model was used in this study. The animals were exposed to 10 mg/kg GaAs, orally, once daily, 5 days a week for 24 weeks and treated thereafter with single oral daily dose of either 0.3 mmol/kg DMSA or MiADMSA for two course of 5 days treatment. The animals were sacrificed thereafter. Lipid peroxidation was assessed by measuring liver thiobarbituric acid reactive substance (TBARS). Liver damage was assessed by number of biochemical variables and by light microscopy. The activity of superoxide dismutase (SOD) and δ-aminolevulinic acid dehydratase (ALAD) beside reduced glutathione (GSH) concentration was measured in blood. Exposure to GaAs produced a significant reduction in GSH while, increased the oxidized glutathione (GSSG) concentration. Hepatic glutathione peroxidase (GPx) and catalase activity increased significantly while level of serum transaminase increased moderately. Gallium arsenide exposure also produced marked hepatic histopathological lesions. Overall, treatment with MiADMSA proved to be better than DMSA in the mobilization of arsenic and in the turnover of some of the above mentioned GaAs sensitive biochemical alterations. Histopathological lesions also, responded more favorably to chelation treatment with MiADMSA than DMSA.

Developmental changes in 7-ethoxyresorufin- O-deethylase (EROD) and δ-aminolevulinic acid dehydratase (ALA-D) activities in three passerines

In this study, we report changes in 7-ethoxyresorufin- O-deethylase (EROD) and δ-aminolevulinic acid dehydratase (ALA-D) enzyme activities during development of three wild passerine bird species: pied flycather ( Ficedula hypoleuca), great tit ( Parus major) and blue tit ( P. caeruleus). Activities were determined from late embryos, newly hatched, 1-week-old and 15-day-old nestlings and adult birds. EROD activity from hepatic microsomes and ALA-D activity from liver tissue and erythrocytes were measured. In all species investigated EROD and ALA-D activities were increased during the first posthatching week and decreased thereafter. Also, differences between activities in late-term nestlings and adults were seen. Based on these results, we suggest that the developmental status of an animal must always be taken into account when evaluating the results obtained in the biomarker studies.

Arsenic-induced changes in certain neurotransmitter levels and their recoveries following chelation in rat whole brain

Arsenic as sodium arsenite (100 ppm in drinking water) was administered to male rats for 16 weeks. Animals were then treated either with meso-2,3-dimercaptosuccinic acid (DMSA), sodium 2,3-dimercaptopropane 1-sulfonate (DMPS), dimethyl DMSA (DmDMSA), or diisopropyi DMSA (DiPDMSA) twice daily (50 mg/kg) intraperitoneally for 5 days. After 5 clays of rest period, the animals were again given a second course of chelation therapy. The animals were sacrificed subsequently for the determination of whole brain biogenic amines levels, acetylcholinesterase (AChE), monoamine oxidasc (MAO) and δ-aminolevulinic acid dehydratase (ALAD) activities. A number of biochemical parameters and arsenic concentrations in some tissues were also determined. The results suggest a significant increase in brain arsenic concentration accompanied by alterations in neurotransmitters levels following As(III) exposure. Although chelation treatment was effective in reducing As burden, the altered biochemical variables responded less favorably to chelation therapy. The DMSA-diesters, particularly DiPDMSA, produced a more pronounced increase in brain arsenic burden, as well as alterations in a few neurotransmitters. It can be concluded that the lipophilic character of As antidotes may lead to unfavorable results following intraperitoneal administration.

Porphyrias in Japan

Porphyrias are a clinically diverse group of diseases due to inherited deficiencies of enzymes in the heme biosynthetic pathway. Much progress has been made in the analysis of porphyrin metabolism, and the molecular biology of the enzymes in heme biosynthesis and their mutations in the porphyrias are now actively investigated. These diseases are classified into two types: erythropoietic and hepatic, depending on the major site of the clinical expression of the enzyme defect. They are further classified into eight subtypes according to the porphyrin metabolites that are over-produced and according to the causative enzyme defects. These diseases are all inherited as autosomal dominant traits, except for congenital erythropoietic porphyria (CEP) and δ-aminolevulinic acid dehydratase (ALAD) deficiency porphyria (ADP), which are recessive. In addition, a few homozygous forms of the dominantly inherited porphyrias have also been recognized, which are presumably due to mutations with a milder enzymatic defect. The main clinical manifestations of the porphyrias are neurologic syndromes and skin photosensitivity.

Distribution of δ-aminolevulinic acid synthetase and δ-aminolevulinic acid dehydratase in liver and kidney of rainbow trout ( Salmo gairdnerii)

1. 1. Activities of δ-aminolevulinic acid synthetase (ALA-S) and δ-aminolevulinic acid dehydratase (ALA-D) in trout liver and kidney were compared with those in the mouse. 2. 2. ALA-S activity (per unit tissue fresh weight) exceeded ALA-D activity in trout liver and kidney. 3. 3. In trout kidney, ALA-S activity slightly exceeded, and ALA-D activity far exceeded, their activities in trout liver. 4. 4. In trout, heme synthesis differs from that in mammals in that appreciable synthesis occurs in the kidney, and in that ALA-S activity in not rate limiting.

Cyanide intoxication—III. On the analogous and different effects provoked by non-lethal and lethal challenged doses

1. 1. The effect of acute cyanide administration to mice in a lethal and a non-lethal dose and the anti-cyanide effect of S- adenosyl- l-methionine (SAM) and thiosulphate were investigated. 2. 2. The poisoning action was determined by measuring cytochrome oxidase, rhodanese and δ-aminolevulinic acid dehydratase (ALA-D) activity. 3. 3. The toxic metabolizing degree was investigated by measuring plasma and urine thiocyanate levels. 4. 4. The state of the sulfane sulfur pool was investigated by determining cyanide labile-sulfur levels. 5. 5. These results support the belief that rhodanese plays a fundamental role in the detoxification process only when high levels of cyanide are administered.

Comparison of inhibition of erythrocyte pyrimidine 5′-nucleotidase and δ-aminolevulinic acid dehydratase by lead

The effect of lead on the activities of erythrocyte pyrimidine 5'-nucleotidase (P5N) and δ-aminolevulinic acid dehydratase (ALAD) was investigated in control and lead-exposed workers. The inhibitory effect of lead in vivo and in vitro was more remarkable on the ALAD than on the P5N activity values. It was demonstrated that the pH optimum of both ALAD and P5N in lead workers shifts to the acidic side (nearly pH 6.0) compared to that in control workers.