Protective Effects of Taif Rosewater Against Testicular Impairment Induced By Lead Intoxication In Rats.

This study explored treatment with Taif rosewater (RW) to protect against lead acetate-(PbAc) induced male testicular impairment. Male Wistar rats were divided into four groups and provided drinking water containing 4% Taif RW, PbAc, 4% Taif RW followed by PbAc or normal water (controls). Serum for hormonal assays and testicular tissue for histopathological and immunohistochemical examinations and molecular study were obtained. Epididymal spermatozoa were collected for analysis. PbAc significantly reduced serum levels of follicle-stimulating hormone (FSH), luteinising hormone (LH) and testosterone, as well as sperm count and motility percentage. It also caused a significant reduction in SOD and catalase activities, testicular CYTP450SCC , CYP17α, StAR mRNA expressions and the percentage of Bcl-2 immunoreactivity. The percentage of caspase-3 and NF-ĸB immunoreactivities, as well as sperm abnormalities, was increased, as did the testicular degeneration associated with vacuolation and necrosis of spermatogenic cells. Pretreatment with Taif RW significantly reduced the negative effects of PbAc as shown by the increases in serum gonadotropins level, SOD and catalase activities, and percentage of Bcl-2 immunoreactivity, decreases in the percentage of caspase-3 and NF-ĸB immunoreactivities, and improved testicular histology and sperm parameters. These data provide evidence that Taif RW protects against testicular toxicity caused by PbAc.

Rare cases of severe life-threatening lead poisoning due to accident or chronic occupational exposure to lead and manganese: Diagnosis, treatment, and prognosis.

BACKGROUND: Chronic long-term, low-dose environmental and occupational exposure to lead (Pb) has been extensively studied in large cohorts worldwide among general populations, miners, smelters, or battery workers. However, studies on severe life-threatening Pb poisoning due to accidental or chronic occupational exposure to Pb and manganese (Mn) were rarely reported. METHODS: We present one case of acute severe Pb poisoning and compare it with another severe chronic occupational exposure case involving Pb and Mn. A 27-year-old woman mistakenly took a large quantity of pure Pb powder as an herbal remedy; she developed abdominal colic, severe nausea, vomiting, fatigue, and cutaneous and sclera icterus. Laboratory tests showed her blood lead level (BLL) of 173.5 µg dL-1 and urinary lead level (ULL) of 1240 µg dL-1. The patient was diagnosed with acute Pb poisoning and acute liver failure. In another chronic exposure case, a 56-year-old man worked in a Pb and Mn smelting factory for 15 years. He was brought to the emergency room with severe nausea, vomiting, and paroxysmal abdominal colic, which was intolerable during the onset of pain. His BLL was 64.8 µg dL-1 and ULL was 38 µg dL-1, but his blood and urinary Mn levels were normal. The patient was diagnosed with chronic Pb poisoning. Both patients received chelation therapy with calcium disodium ethylene-diamine-tetraacetate (CaNa2EDTA). The woman with acute severe Pb intoxication recovered well and was discharged from the hospital after treatment, and the man who survived severe Pb poisoning was diagnosed with lung cancer. CONCLUSION: Clinical manifestations of acute and chronic severe Pb poisoning are different. Chelation therapy with CaNa2EDTA is proven to be an effective life-saving therapy in both cases by reducing BLL. Occupational exposure to both Pb and Mn does not appear to increase Mn neurotoxicity; however, the probability that co-exposure to Mn may increase Pb toxicity in the same patient cannot be excluded.

Lead exposure induces metabolic reprogramming in rat models.

Lead is a toxin of great public health concern affecting the young and aging population. Several factors such as age, gender, lifestyle, dose, and genetic makeup result in interindividual variations to lead toxicity mainly due to variations in metabolic consequences. Hence, the present study aimed to examine dose-dependent lead-induced systemic changes in metabolism using rat model by administering specific doses of lead such as 10 (low lead; L-Pb), 50 (moderate lead; M-Pb), and 100 mg/kg (high lead; H-Pb) body weight for a period of one month. Biochemical and haematological analysis revealed that H-Pb was associated with low body weight and feed efficiency, low total protein levels (p ≤ 0.05), high blood lead (Pb-B) levels (p ≤ 0.001), low ALAD (δ-aminolevulinate dehydratase) activity (p ≤ 0.0001), high creatinine (p ≤ 0.0001) and blood urea nitrogen (BUN) (p ≤ 0.01) levels, elevated RBC and WBC counts, reduced haemoglobin and blood cell indices compared to control. Spatial learning and memory test revealed that H-Pb exposed animals presented high latency to the target quadrant and escape platform compared to other groups indicating H-Pb alters cognition function in rats. Histopathological changes were observed in liver and kidney as they are the main target organs of lead toxicity. LC-MS analysis further revealed that Butyryl-L-carnitine (p ≤ 0.01) and Ganglioside GD2 (d18:0/20:0) (p ≤ 0.05) levels were significantly reduced in H-Pb group compared to all groups. Further, pathway enrichment analysis revealed abundance and significantly modulated metabolites associated with oxidative stress pathways. The present study is the first in vivo model of dose-dependent lead exposure for serum metabolite profiling.

Air, water, soil and environmental signaling.

Within a remarkably short timespan the world population doubled and transitioned from an agrarian to an urban-industrial society. The transition was accompanied by the major expansion of industries that releases enormous amounts of toxicants into the air, water, and soil. Naturally occurring and synthetic chemicals compounds utilized the same signaling system as vertebrate internal cell signaling systems. The concept of environmental signals provides insights to address the impact of biochemically active toxicants on humans and the ecosystems that they share with other species. Disruption of the broad signaling systems has the potential for global change that transcends the biological systems of all organisms, including humans.

Impacts of lead exposure and chelation therapy on bone metabolism during different developmental stages of rats.

OBJECTIVE: To explore the impacts of Pb exposure and the dimercaptosuccinic acid (DMSA) chelation therapy on bone metabolisms in young rats of different ages, as well as the potential mechanisms. METHOD: Young rats were exposed to 0.05%-0.1% Pb acetate for 19 days, during infanthood (postnatal day, PND2-20), childhood (PND21-39) and adolescenthood (PND40-58) respectively. In each developmental stage, rats were further divided into three subgroups: lead-exposed, one-course and two-course DMSA chelation therapy subgroups. Blood/bone lead concentrations, serum calciotropic hormones concentrations, and mRNA and protein expressions of bone turnover markers in the serum and bones were measured. Bone microstructures were analyzed using Micro-CT. RESULTS: Compared with lead-exposed during childhood and adolescenthood, increases in blood/bone lead levels, and the changes of blood/bone lead and trabecular bone microstructures after one-course DMSA chelation were most significant in rats lead-exposed during infanthood (P < .05). The serum osteocalcin (OC) concentrations, mRNA/protein expressions of OC and runt-related transcription factor 2 (RUNX2) in bones all decreased after Pb exposure, along with significant increases in serum C-terminal telopeptide of type I collagen (CTX) concentrations (P < .05). These effects were accompanied by changes of serum parathormone (PTH) and 1,25-dihydroxyvitamin D3 (1,25-(OH2)-D3) concentrations. DMSA chelation partially reversed the changes of bone microarchitectures, bone formation and resorption markers, and calciotropic-hormones, and the efficiency was greatest when the therapy was provided during infanthood. CONCLUSION: Developmental Pb exposure impaired bone microstructures and interfered bone metabolism, and the exposure effect was more obvious during infanthood than during childhood and adolescenthood. Lead effects were partially reversed by chelation therapy, and the efficacy may be most significant when the therapy was provided at younger ages.

Chronic occupational exposure to lead leads to significant mucocutaneous changes in lead factory workers.

BACKGROUND: Chronic lead toxicity is a worldwide public health problem. Lead possesses deleterious effects on many organ systems. However, little is known regarding its clinical and biophysical effects on the skin. OBJECTIVE: To investigate mucocutaneous signs and biophysical property changes in skin after chronic lead toxicity. METHODS: One hundred and eighty-seven patients who were car battery workers participated in the study. Complete history and physical examination were performed. Blood was collected for laboratory analyses. Thorough skin examination by dermatologists was carried out in 134 subjects. Additionally, 96 patients with blood lead levels (BLL) >70 µg/dL were further evaluated for skin elasticity, sebum content, transepidermal water loss (TEWL), hydration, pH and pigmentation. An equal number of age-, sex- and skin-type-matched subjects were recruited as controls. RESULTS: The mean BLL of all subjects was 74.15 ± 11.58 µg/dL. The most frequently observed signs were gingival brown pigmentation in 112 (83.6%), gingivitis in 111 (82.8%) and lead line in 66 (49.3%) patients. The lead line was found in subjects with significantly higher BLLs (adjusted mean difference 6.45, 95% CI 2.30-10.60 µg/dL, P = 0.003) and in association with gingivitis (adjusted OR 7.32, 95% CI 2.08-25.74, P = 0.002). Mean BLL of the patients who underwent biophysical assessment was 82.77 ± 9.80 µg/dL. Patients exhibited a statistically significant lower skin hydration observed by corneometer as well as elasticity. The adjusted ORs of having dry skin and lower elasticity were 15.32 (95% CI 4.41-53.24), P < 0.001) and 1.96 (95% CI 1.06-3.60), P = 0.031), respectively. These differences were not significant for sebum content, TEWL, pH and pigmentation. CONCLUSION: Importantly, even in normal-appearing skin, level of hydration and elasticity decreased in lead-intoxicated patients. These results suggest that lead might possess harmful effects on the skin at measurable levels.

Outbreak investigation of lead neurotoxicity in children from artificial jewelry cottage industry.

BACKGROUND: Although lead neurotoxicity is a known phenomenon, it can often be missed at a primary or secondary care level especially if detailed environmental exposure history is missed. METHODS: This is an outbreak investigation where we observed 15 pediatric cases with neurologic signs and symptoms clustered in a slum area known for an unorganized artificial jewelry industry. Their clinical, biochemical, and epidemiological features were compared with 14 other children from the same region reporting with non-neurological symptoms who were considered as unmatched controls. RESULTS: Cases with neurological manifestations had a higher in-house lead smelting activity [OR 7.2 (95% CI 1.4-38.3)] as compared to controls. Toddlers below 3 years of age were more vulnerable to the effects of lead. CONCLUSION: This study emphasizes that many focal sources of lead poisoning still remain especially in the unorganized sector. In cases presenting with unexplained neurotoxicity, specific occupational and environmental inquiry for chemical poisoning, with special consideration for lead, should be actively pursued.

The effects of occupational lead exposure on selected inflammatory biomarkers.

In exposure to toxic metals such as lead, determining lead and cytokine levels (IL-6, IL-10, and TNF-α) is essential for early detection of diseases. The aim of this study was to develop an model for early detection of inflammation and onset of atherosclerosis in the absence of clinical findings in young workers, which could help physicians take timely an action and start treatment. This study included 49 metal workers exposed to lead occupationally and 50 unexposed administrative workers (controls) who underwent immunological analysis for cytokines (IL-6, IL-10, and TNF-α) and atherosclerosis markers (h-FABP and VCAM-1), toxicological analysis for lead, and routine biochemical analysis (ALT, AST, creatinine) at the Ankara Occupational and Environmental Diseases Hospital in 2017. Lead levels correlated with IL-6, IL-10, and TNF-α (r=0.469, r=0.521 and r=0.279, respectively, p<0.01) but did not significantly affect h-FABP and VCAM-1 levels.

Contribution of Fetal Programming in the Formation of Cognitive Impairments Induced by Lead Poisoning in White Rats.

The contribution of prenatal hypoxic damage to the CNS to the formation of high sensitivity of the body to lead acetate was studied. Prenatal fetal hypoxia was modeled by the administration of sodium nitrite in doses of 5, 25, and 50 mg/kg to pregnant female rats. Cognitive capacities of mature offspring were evaluated in the radial maze test and Morris water maze test. After attaining learning criterion in the radial maze, lead acetate in a dose of 80 mg/kg was added to the drinking water of all animals over 2 weeks. Testing was performed during the exposure to the agent until disruption of the conditioned behavior. It was found that severe prenatal hypoxia (induced by the administration of 50 mg/kg sodium nitrite) impaired spatial memory, increased latency of funding the platform in Morris water maze test, and serves as a factor contributing to earlier manifestations of the neurotoxic effects of lead acetate.

ECG conduction disturbances and ryanodine receptor expression levels in occupational lead exposure workers.

OBJECTIVES: A significant number of researches have evidenced that occupational lead (Pb) exposure increased risks of cardiovascular disease. However, evidences about the potential effects of Pb on the cardiac conduction system are sparse and inconclusive. Besides, ryanodine receptors (RyRs) induced dysfunction of cardiac excitation contraction coupling which is considered to be one of the mechanisms in cardiovascular diseases. Therefore, we examined the association between occupational Pb exposure and ECG conduction abnormalities, as well as RyRs in Pb-induced ECG abnormalities. METHODS: We investigated 529 Pb smelter workers, and measured blood lead (BPb), zinc protoporphyrin (ZPP), ECG outcomes and RyR expression levels. Based on BPb levels, the workers were divided into three groups: the BPb not elevated group, the BPb elevated group and the Pb poisoning group. Descriptive and multivariable analyses were performed. RESULTS: Compared with the BPb not elevated group, the Pb poisoning group had a higher incidence of high QRS voltage, and a lower level of RyR1 gene expression (p<0.05). Further unconditional multivariable logistic regression analyses showed that high QRS voltage was positively related to BPb (OR=1.045, 95% CI 1.014 to 1.078) and inversely associated with RyR1 expression (OR=0.042, 95% CI 0.002 to 0.980) after adjusting for potential confounders. In addition, multiple linear regression analyses showed that the QTc interval was positively associated with ZPP (ß=0.299, 95% CI 0.130 to 0.468) after adjusting for potential confounders. CONCLUSIONS: Our study provided evidences that occupational exposure to Pb may be associated with worse ECG outcomes (high QRS voltage), which might be related to decreased levels of RyR1.

Impact of chronic lead exposure on liver and kidney function and haematologic parameters.

BACKGROUND: Lead, one of the most widely used metals because of its beneficial physical properties, has been reported to adversely influence several different organs and organ systems. The aim of the present study was to examine the effect of lead exposure on liver and renal function and haematologic parameters. METHODS: This was a case-cohort study comparing adults with occupational, environmental or opium-related lead exposure with blood lead levels [BLL] >10 µg/dL (High blood lead level (HBLL) group and age- and gender-matched normal healthy individuals (Low blood lead level [LBLL] group with BLL <10 µg/dL). The complete blood count and concentrations of serum creatinine, urea, aspartate aminotransferase (AST), alanine aminotransferase (ALT) were recorded for subsequent investigation. RESULTS: The mean BLL was significantly higher in the HBLL than in the LBLL groups (51.36 ± 44.72 vs 4.17 ± 1.97 µg/dL). The Spearman's rho revealed a significant association between BLL and urea (r = 0.25, P < 0.001), creatinine (r = 0.16, P = 0.02), AST (r = 0.42, P < 0.001) and ALT (r = 0.27, P < 0.001). The median [IQR] serum urea (34 mg/dL [27-221]) vs (30 [27-36]), creatinine (0.9 mg/dL [0.8-1]) vs (0.8 [0.7-0.9]), ALT (25 mg/dL [16-49]) vs (22 [16-30]) and AST concentrations (29 mg/dL [20-42]) vs (20 [18-24]) were all significantly higher (P < 0.05) in the HBLL group compared to the LBLL group. The median [IQR] haemoglobin (12.6 g/dL [10.4-15.4]) vs (15.2 [14.6-16.3] and haematocrit (36.9% [31-44.8]) vs (45.6 [43.6-48.2]) were both significantly lower (P < 0.001) in the HBLL group than in the LBLL group. CONCLUSION: The results indicated that people with chronic lead exposure with BLLs greater than 10 µg/dL are at risk of renal, liver and haematologic impairments.

The role of the South African Medical Research Council in reducing lead exposure and preventing lead poisoning in South Africa.

Even at low levels in blood, lead has been associated with reduced IQ scores, behavioural problems, learning impediments, aggression and violent behaviour. Since the 1980s, the South African Medical Research Council (SAMRC) has been investigating the sources of exposure to lead in South Africa (SA), the groups at highest risk of lead poisoning and a selection of the myriad associated health and social consequences. SAMRC research evidence contributed to the phasng out of leaded petrol, restrictions on lead in paint and other interventions. Subsequently, childhood blood lead levels in SA declined significantly. More recent studies have revealed elevated risks of lead exposure in subsistence fishing and mining communities, users of arms and ammunition, those ingesting certain traditional medicines, and users of certain ceramicware and artisanal cooking pots. Lead-related cognitive damage costs the SA economy ~USD17.7 (ZAR261.3) billion annually, justifying further SAMRC investment in lead exposure research in the country.

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.

Effects of short term lead exposure on gut microbiota and hepatic metabolism in adult zebrafish.

Lead (Pb) is one of the most prevalent toxic, nonessential heavy metals that has been associated with a wide range of toxic effects in humans and environmental animals. Here, effects of short time exposure to 10 and 30 µg/L Pb on gut microbiota and hepatic metabolism were analyzed in adult male zebrafish. We observed that both 10 and 30 µg/L Pb increased the volume of mucus in the gut. At phylum level, the abundance of α-Proteobacteria decreased significantly and the abundance of Firmicutes increased significantly in the gut when treated with 30 µg/L Pb for 7 days. In addition, the 16S rRNA gene sequencing for V3-V4 region revealed a significant change in the richness and diversity of gut microbiota in 30 µg/L Pb exposed group. A more depth analysis, at the genus level, discovered that 52 gut microbes identified by operational taxonomic unit analysis were changed significantly in 30 µg/L Pb treated group. Based on GC/MS metabolomics analysis, a total of 41 metabolites were significantly altered in 30 µg/L Pb treatment group. These changed metabolites were mainly associated with the pathways of glucose and lipid metabolism, amino acid metabolism, nucleotide metabolism. In addition, we also confirmed that the transcription of some genes related to glycolysis and lipid metabolism, including Gk, Aco, Acc1, Fas, Apo and Dgat, decreased significantly in the liver of zebrafish when exposed to 30 µg/L Pb for 7 days. Our results observed that Pb could cause gut microbiota dysbiosis and hepatic metabolic disorder in zebrafish.

Lead-interacting proteins and their implication in lead poisoning.

Lead is an important heavy metal used worldwide in several applications, especially in industry. People exposed to lead can develop a wide range of symptoms associated with lead poisoning. Many effects of lead poisoning are reported in the literature, showing a compromising of whole body health, with symptoms related to cardiovascular, immune, bone, reproductive, hematological, renal, gastrointestinal, and nervous system. However, the molecular lead targets as well as the pathways affected by lead poisoning are not completely described. The aim of this study was to construct a map of metabolic pathways impaired in lead poisoning by evaluating which biomolecules are directly affected by lead. Through manual literature curation, we identified proteins which physically interact with lead and subsequently determined the metabolic pathways those proteins are involved with. At total, we identified 23 proteins involved with heme synthesis, calcium metabolism, neurotransmission, among other biological systems, which helps to understand the wide range of lead-poisoning symptoms.

Lead inhalation and hepatic damage: Morphological and functional evaluation in mice.

Lead (Pb) is a heavy metal that plays an unknown biological role and is very toxic even at low concentrations. The main sources of Pb are Pb-contaminated areas in industrial areas or landfills. Inhalation is one of the most common routes of exposure to this metal, but there is little information on its effect on the liver. Thirty male mice were exposed to 0.1 M Pb acetate by inhalation for 8 weeks, twice a week for 1h. A recovery group was free of exposure for 4 weeks. Histological evaluation showed an increase in the inflammatory infiltrate and in the percentage of meganuclei in the liver. This was observed since the first week and throughout the whole exposure time. A significant increase in the aspartate aminotransferase concentration was observed in the liver function tests; yet, the alanine aminotransferase concentration did not show significant changes. The 4-hydroxynonenal (4-HNE) and nitrotyrosine levels in Pb-exposed mice, identified by immunohistochemistry, showed a significant increment compared to the controls. This effect was observed throughout Pb exposure. After a 4-week period of suspended exposure, recovery time, the concentration of 4-HNE and nitrotyrosine decreased to similar levels of those previously observed in controls, this suggests a decrease in the generation of oxidative stress by Pb inhalation. Although our results suggest that the lungs are the first contact organs and filters during Pb inhalation, this metal eventually reaches the liver and might cause damage by oxidative stress. This damage can decrease in time if exposure is discontinued.

[Study on the health effects of occupational exposure to lead exceeded].

Objective: The main purpose of this study was to explore the health effects of occupational exposure to lead exceeded. Methods: We collected 114 inpatients who exposure to lead, and diagnosed lead toxicity by No. 5 Suzhou People's Hospital from January 2011 to May 2018. Samples were selected according to 1:4 of the lead exceeded group and the control group. The age and gender of the lead exce eded group were matchied, and balanced between the two groups. Lead exceeded group: 84 inpatients occupational exposure to lead, whose blood or urinary lead exceeded. Control group: 336 healthy checkup persons who did not contact with any toxic or hazardous substances. Results: The diastolic blood pressure of lead exceeded group was significantly higher than control group (P<0.05) . The red blood cell count, hemoglobin, mean red blood cell volume, mean hemoglobin content, mean hemoglobin concentration, the platelet count, and the lymphocyte count levels of lead exceeded group were significantly lower than control group (P<0.05) , while the average platelet volume level of lead exceeded group was significantly higher than control group (P<0.05) . The aspartate aminotransferase, glucose and the urea nitrogen levels of lead exceeded group were significantly higher than control group, while the creatinine of lead exceeded group was significantly lower than control group (P<0.05) . The total protein, albumin, cholesterol and low density lipoprotein levels of lead exceeded group were significantly lower than control group (P<0.05) . The abnormal rate of electrocardiogram and spleen B (24.4%, 8.33%) in lead exceeded group were significantly higher than control group (11.04%, 0.6%) (P<0.05) . The abnormal rate of liver B ultrasound, and gallbladder B ultrasound (23.81%、8.32%) in lead exceeded group were significantly lower than control group (41.32%、21.06%) (P<0.05) . Conclusion: Occupational exposure to lead exceeded not only has a significant impact on red blood cell related indicators, but also has a certain impact on cardiac function and liver and kidney functions. It is suggested that lead exprsure may have some effect on health of occupational population.

Role of geraniol against lead acetate-mediated hepatic damage and their interaction with liver carboxylesterase activity in rats.

In this study, the effect of geraniol (50 mg/kg for 30 d), a natural antioxidant and repellent/antifeedant monoterpene, in a rat model of lead acetate-induced (500 ppm for 30 d) liver damage was evaluated. Hepatic malondialdehyde increased in the lead acetate group. Reduced glutathione unchanged, but glutathione S-transferase, glutathione reductase, as well as carboxylesterase activities decreased in geraniol, lead acetate and geraniol + lead acetate groups. 8-OhDG immunoreactivity, mononuclear cell infiltrations and hepatic lead concentration were lower in the geraniol + lead acetate group than the lead acetate group. Serum aspartate aminotransferase and alanine aminotransferase activities increased in the Pb acetate group. In conclusion, lead acetate causes oxidative and toxic damage in the liver and this effect can reduce with geraniol treatment. However, we first observed that lead acetate, as well as geraniol, can affect liver carboxylesterase activity.

Detection of DNA Fragmentation in Liver of Goats Exposed to Lead Poisoning in Bagega District of Zamfara State, Nigeria.

The ubiquitous presence of lead (Pb) and its release by anthropogenic activities has remained a majorenvironmental pollution risk to both humans and animals. Lead toxicity has been associated with different systemic toxicitiesand biochemical impacts (such as oxidative stress and DNA damaging effects) with dire health consequences. In Nigeria,the health problem associated with lead toxicity has been overwhelming in the Bagega District of Zamfara State whereartisanal gold mining has resulted in widespread environmental lead contamination. For this study, 24 goats were selectedfrom two communities, 12 goats (exposed groups) selected from Bagega District, Zamfara (a community with widespreadmining and lead contamination), while 12 goats (control) were selected from Apete, Ibadan with no previous mining history.The liver lead levels in the two groups were evaluated using the using Atomic Absorption Spectrophotometry and the leadlevel in the exposed group was categorized into 3 exposure categories (viz mild, moderate and severe). Representative liversamples from the 3 tissue lead exposure categories were analyzed using agarose gel electrophoresis for the detection ofapoptotic oligonucleosomal DNA fragmentation. The tissue lead level in the goats from the exposed group (32.42±13.85mg/kg) was significantly higher than the control group (0.36±0.12 mg/kg). DNA ladder was detected in the 3 exposure categories with a dose-related degree of DNA fragmentation. This study highlights the role of oligonucleosomal DNAfragmentation and apoptosis in the pathogenicity of lead in lead exposed goats and the associated the dose-gradient impactof tissue lead level on the degree of DNA fragmentation.