Ameliorating Effect of Apium graveolens (Celery) Extracts on IL-6 Plasma Level and Expression of Caspase 3 on Liver in Animal Model of Lead Intoxication.

<b>Background and Objective:</b> Lead poisoning (Pb) is a big problem because it is found in almost all objects in daily life such as vehicle fuel, water pipes, ceramics, cosmetics and others. Continuous lead exposure can increase ROS resulting in an increase in hepatic IL-6 and caspase 3 which replaces hepatic cell apoptosis. The objective of this study was to determine the effect of <i>Apium graveolens</i> (celery) extract on plasma IL-6 and hepatic caspase 3 levels. <b>Materials and Methods:</b> This study used a post-test control group design. The research subjects were 20 Wistar rats that met the inclusion criteria and were divided into 4 groups randomly, namely (a) Sham group that had no treatment, (b) Negative control group was induced with lead acetate 200 mg kg¹ body weight/day without any treatment (c) Positive control group and (d) Treated group. On the 15th day, blood was taken to check IL-6 levels and tissue was taken for liver caspase 3 examination by immunohistochemical method. Data analysis used the one-way ANOVA test and continued with the <i>post hoc</i> LSD test. <b>Results:</b> The highest mean caspase 3 expression was in the control group 45.84±4.39 pg mL¹, while the mean of IL-6 plasma level was highest in the P1 641.33±39.72 pg mL¹ group. The Mann-Whitney test showed a significant difference in IL-6 levels between the study groups (p = 0.000). The Mann-Whitney test showed a significant difference in caspase 3 levels between the study groups (p = 0.000). <b>Conclusion:</b> Giving celery extract 300 mg kg¹ body weight/day affects plasma IL-6 and hepatic caspase 3 levels in lead acetate-induced rats.

Lead toxicity and potential therapeutic effect of plant-derived polyphenols.

BACKGROUND: Due to its unique physical and chemical properties, lead is still used worldwide in several applications, especially in industry. Both environmental and industrial lead exposures remain a public health problem in many developing and rapidly industrializing countries. Plant polyphenols are pleiotropic in their function and have historically made a major contribution to pharmacotherapy. PURPOSE: To summarize available pre-clinical and limited clinical evidence on plant polyphenols as potential antidotes against lead poisoning and discuss toxic mechanisms of lead. METHOD: A comprehensive search of peer-reviewed publications was performed from core collections of electronic databases such as PubMed, Web of Science, Google Scholar, and Science Direct. Articles written in English-language from inception until December 2022 were selected. RESULTS: In this review, we review key toxic mechanisms of lead and its pathological effects on the neurological, reproductive, renal, cardiovascular, hematological, and hepatic systems. We focus on plant polyphenols against lead toxicity and involved mechanisms. Finally, we address scientific gaps and challenges associated with translating these promising preclinical discoveries into effective clinical therapies. CONCLUSION: While preclinical evidence suggests that plant polyphenols exhibit bioprotective effects against lead toxicity, scant and equivocal clinical data highlight a need for clinical trials with those polyphenols.

Essential Trace Metals as Countermeasure for Lead Toxicity.

Lead (Pb) is the most common toxic heavy metal that is physiologically non-essential and imposes health complications in animals and humans. Chelation therapy is considered as the definite therapy for acute lead toxicity; clinical uses of chelating agents are not recommended in long-term lead toxicity and in children. Research reveals that essential trace metals can counteract empirical Pb toxicity. This article collates the prototypical evidence of the preventive action of essential trace metals towards Pb toxicity in animals. Zinc, selenium, and their combinations are effective here. The key mechanisms of homeostasis of essential metals and cytoprotection are: modulation of signal transduction pathways of apoptosis, inflammation and immune functions (for selenium), attenuation of oxidative stress by augmenting non-enzymatic and enzymatic antioxidative systems and interference in lead accumulation in the body. By means of these mechanisms, these essential trace metals may counteract long-term lead toxicity for susceptible subjects. These mineral nutritional supplementation can easily be employed with no or less adverse effects compared to the typical chelation treatment.

Abdominal pain caused by lead toxicity due to over the counter herbal medicines: A case series.

In the last three decades, the use of herbal medications has been increasing for the treatment of various chronic disorders. Studies in the past have shown that many of these medicines could contain high levels of heavy metals, including lead. Therefore, we planned this study to evaluate the possibility of lead toxicity as the underlying cause in patients consuming these unnamed herbal medicines among patients presenting with significant abdominal pain. (Unexplained abdominal pain means pain in abdomen in which no etiology could be ascertained after all possible routine and specialized investigations including computerized axial tomography [CT] of the abdomen and upper gastrointestinal [UGI] endoscopy/colonoscopy). This is an observational case series of prospectively maintained data of all patients having unexplained abdominal pain and found to have an elevated blood lead level from 2011 to 2019. Lead toxicity was diagnosed when its blood lead level was >25 µg/dL. Total sixty-six patients with unexplained abdominal pain from 2011 to 2019 were recruited. Out of the sixty-six patients, seventeen had elevated blood lead levels. All seventeen patients had a history of ingestion of herbal medicines for more than 6 months. Among the seventeen patients, eight were taking it for infertility and sexual dysfunction, six for diabetes, two for arthritis and one for hypertension. Basophilic stippling was seen in one patient. Fourteen patients had low hemoglobin with a median value of 9.7 g/dL. Mean serum blood lead level was 87.1 µg/dL. None of them required anti-chelating agent. Lead toxicity owing to herbal medicine is not uncommon cause of unexplained abdominal pain. Most of these patients do not require a chelating agent for treatment. There is a need to bring these herbal medicines under strict regulations for displaying its constituents and their concentrations.

A systematic review of clinical and laboratory findings of lead poisoning: lessons from case reports.

Lead is one of the most toxic heavy metals in the environment. The present review aimed to highlight hazardous pollution sources, management, and review symptoms of lead poisonings in various parts of the world. The present study summarized the information available from case reports and case series studies from 2009 to March 2020 on the lead pollution sources and clinical symptoms. All are along with detoxification methods in infants, children, and adults. Our literature compilation includes results from 126 studies on lead poisoning. We found that traditional medication, occupational exposure, and substance abuse are as common as previously reported sources of lead exposure for children and adults. Ayurvedic medications and gunshot wounds have been identified as the most common source of exposure in the United States. However, opium and occupational exposure to the batteries were primarily seen in Iran and India. Furthermore, neurological, gastrointestinal, and hematological disorders were the most frequently occurring symptoms in lead-poisoned patients. As for therapeutic strategies, our findings confirm the safety and efficacy of chelating agents, even for infants. Our results suggest that treatment with chelating agents combined with the prevention of environmental exposure may be an excellent strategy to reduce the rate of lead poisoning. Besides, more clinical studies and long-term follow-ups are necessary to address all questions about lead poisoning management.

Resveratrol reverses hippocampal synaptic markers injury and SIRT1 inhibition against developmental Pb exposure.

Lead (Pb) exposure damages synaptic structural plasticity that results in cognitive impairment. Resveratrol, a natural polyphenolic compound, is one of the most potent agonists of silencing information regulator 1 (SIRT1) discovered to date. However, the effects of SIRT1 on synaptic functional plasticity in early life Pb exposure are not well studied. Herein, the purpose of this study is to investigate the expression of synaptic markers and SIRT1 in rats exposed to Pb and to evaluate the regulatory effect of resveratrol during this process. The Pb exposed male SD pups were treated with resveratrol (50 mg/kg/d) or EDTA (150 mg/kg/d) followed by hippocampal and blood sampling for analysis at postnatal day 21 (PND21). In the Morrris water maze test, resveratrol treatement protected the rats against Pb-induced impairment of learning and memory (P < 0.05). Resveratrol also enhanced the expression of brain-derived neurotrophic factor (BDNF, P < 0.001 vs 0.2% Pb group), and reversed the effects of Pb exposure on SIRT1(P < 0.001 vs 0.2% Pb group). The DG, CA1 and CA3 regions of the hippocampus showed a considerable increase in the expression of pre- and postsynaptic proteins (P < 0.001 vs 0.2% Pb group). In conclusion, our study demonstrated that resveratrol, through the activation of SIRT1, played a protective role against Pb-induced defects in synaptic plasticity, and suggested a new potential adjuvant treatment for Pb poisoning.

Harnessing Peptides against lead pollution and poisoning: Achievements and prospects.

Among the broad applicability of peptides in numerous aspects of life and technologies, their interactions with lead (Pb), one of the most harmful substances to the environment and health, are constantly explored. So far, peptides were developed for environmental remediation of Pb-contaminations by various strategies such as hydrogelation and surface display. They were also designed for Pb detection and sensing by electrochemical and fluorescent methods and for modeling natural proteins that involve in mechanisms by which Pb is toxic. This review aims at summarizing selected examples of these applications, manifesting the enormous potential of peptides in the combat against Pb pollution. Nevertheless, the absence of new medicinal treatments against Pb poisoning that are based on peptides is noticeable. An overview of previous achievements utilizing Pb-peptide interactions towards various goals is presented and can be therefore leveraged to construct a useful toolbox for the design of smart peptides as next-generation therapeutics against Pb.

Changes in inflammatory cytokines, antioxidants and liver stiffness after chelation therapy in individuals with chronic lead poisoning.

BACKGROUND: Chronic exposure to lead causes lead to accumulate mainly in the liver. In vivo studies have shown that lead toxicity is related to alterations in the inflammatory response. We aimed to evaluate the association between lead poisoning and liver fibrosis as well as the change in the degree of liver fibrosis, levels of inflammatory mediators and glutathione (GSH) after chelation therapy. METHODS: Workers from a battery factory who were exposed to lead for > 12 months and had a blood lead level (BLL) > 70 µg/dL were enrolled (n = 86) in the study. Participants underwent chelation therapy with intravenous CaNa2EDTA for 2 days followed by treatment with oral D-penicillamine for 90 days. The primary outcome was the change in the degree of liver fibrosis, which was presented as liver stiffness (LS) measured by FibroScan®. Secondary outcomes were the changes in the levels of serum GSH and inflammatory mediators such as tumor necrosis factor-alpha (TNF-α), interleukin-1ß (IL-1ß), and interleukin-6 (IL-6) after chelation therapy. RESULTS: Among the 86 participants, there was a positive correlation between the duration of lead exposure and LS (r = 0.249, p = 0.021). To avoid the confounding effect of obesity-related steatosis, only 70 individuals who had controlled attenuation parameters < 296 dB/m, BMI < 25 kg/m2 and normal waist circumference were included in the interventional analysis. After chelation, the mean LS significantly decreased from 5.4 ± 0.9 to 4.8 ± 1.4 kPa (p = 0.001). Similarly, all of the inflammatory cytokines studied significantly decreased after chelation (p < 0.001); TNF-α decreased from 371.6 ± 211.3 to 215.8 ± 142.7; the levels of IL-1ß decreased from 29.8 ± 1.7 to 25.9 ± 4.3; and the levels of IL-6 decreased from 46.8 ± 10.2 to 35.0 ± 11.9. On the other hand, the mean GSH level increased significantly from 3.3 ± 3.3 to 13.1 ± 3.7 (p < 0.001) after chelation therapy. CONCLUSION: The duration of lead exposure was significantly correlated with the degree of liver fibrosis. Chelation treatment was associated with increased levels of GSH and decreased levels of proinflammatory cytokines and could potentially reduce the degree of LS. TRIAL REGISTRATION: This study was retrospectively registered and approved by the Thai Clinical Trial Registry (TCTR) on 2019-11-07. The TCTR identification number is TCTR20191108001 .

Zhiqi Granules Decreased Lead Level but Increased Iron Level in Serum of Chinese Children with Moderately Elevated Blood Lead Levels.

To observe and compare the effects of healthy instruction and Zhiqi granules on lead, calcium, iron, and zinc levels in serum of children with moderately elevated blood lead levels (BLLs). At the same time, the possible mechanisms were discussed. A total of 60 eligible boys aged 4-6 years were selected and divided into two groups (the healthy instruction group and the Zhiqi group) randomly. The boys in the healthy instruction group only received the healthy instruction. Besides the healthy instruction, the boys in the Zhiqi group received 2 g Zhiqi granules orally one time daily. The study lasted for 4 weeks. BLL and serum iron, zinc, and calcium levels of the subjects in the two groups before and after interventions were measured and compared. After the interventions, the BLL in the Zhiqi group lowered significantly, but the decrease of the BLL in the healthy instruction group is not significant, and there was a significant difference in the BLL between the two groups. When the trial was completed, the serum iron level in the Zhiqi group increased significantly, but that in the healthy instruction group changed slightly, and a significant difference was seen between the two groups. There were no significant differences in both serum Ca and Zn levels in these two groups before and after the interventions. Meanwhile, there were no significant differences in serum Ca and Zn levels between the two groups after the interventions. The results suggested that daily intake of Zhiqi granules for 4 weeks together with healthy instruction resulted in a decrease of the BLL and an elevation of the serum iron level.

Malus micromalus Makino phenolic extract preserves hepatorenal function by regulating PKC-α signaling pathway and attenuating endoplasmic reticulum stress in lead (II) exposure mice.

Lead (Pb), which widely recognized as a nonessential heavy metal and a major environmental contamination, is a growing threat to the ecosystem and human body. In the present study, Malus micromalus Makino cv. 'Dong Hong' phenolic extract (MMPE) has been used to antagonise Pb-induced erythrocyte injury, hepatic and renal dysfunction in mice. Six-week-old male Kunming mice were gavaged with PbCl2 (20 mg/kg mouse/day) and/or MMPE (100 mg/kg mouse/day) by gavage administration for 10 days. We evaluated erythrocyte fragility, relative organ mass, biochemical parameters and histopathological changes to evaluate the protection effect of MMPE on the injury of liver and kidney in Pb-treated mice. MMPE significantly inhibited the increase of protein kinase C-α, B-cell lymphoma-2-associated X, cytochrome C and Caspase-3 protein levels and decreased calreticulin protein expression level in Pb-exposed mice. MMPE supplementation could maintain the integrity of erythrocyte membranes and ameliorate the endoplasmic reticulum stress in Pb-treated mice. It suggested MMPE as a natural nutritional supplement to alleviate Pb-induced hazardous effects in Pb-exposed humans.

Effects of combined administration of calcium, iron, zinc, chrysanthemum flavonoids, and DMSA on the treatment of lead intoxication in mice.

The effect of combined administration of calcium (Ca), iron (Fe), zinc (Zn), chrysanthemum flavonoids, and meso-2,3-dimercaptosuccinic acid (DMSA) on the treatment of lead (Pb) intoxication in mice was studied. One hundred ninety female mice (SPF level, aged 18-22 days) were randomly divided into two groups as experimental animals. Mice in group I (10 mice) served as normal control animals, and were administered deionized water containing 12.5 µL/L acetate acid for 6 weeks, whereas mice in group II (180 mice) were exposed to 0.1% (wt/vol) of lead acetate in deionized water for 6 weeks and served as experimental animals. After 6 weeks of successful modeling, 180 mice from group II (lead-exposed) were divided into 18 groups of 10 mice each, 16 of which were treated by the combined administration of Ca, Fe, Zn, chrysanthemum flavonoids, and DMSA by L16 (215 ) orthogonal design. The remaining two groups were given treatment with low and high doses of DMSA, respectively. After three weeks of intervention (ig), the optimal treatment group was identified according to its blood lead level, as well as some antioxidant indices in the blood, liver, and hippocampus. The results indicated that the combined administration of Fe, Zn, chrysanthemum flavonoids, and DMSA with low dosage had the most significant effect on increasing the activities of blood delta-aminolevulinic acid dehydratase and superoxide dismutase (SOD), hepatic SOD and hippocampus nitric oxide synthase while decreasing the blood lead level, the content of hepatic malondialdehyde and hippocampus nitric oxide; this was considered the optimal treatment group. There was no difference in the level of blood hemoglobin between the optimal treatment group and the model control group (the first group of the orthogonal experiment). The activities of blood glutathione (GSH), hepatic GSH and glutathione peroxidase of the optimal treatment group were the same as other groups', and the recovery of the related indexes in the optimal effect group closely resembled the high dosage DMSA group. It can be concluded that the coadministration of Fe, Zn, and chrysanthemum flavonoids along with a low-dose DMSA effectively reduces Pb poisoning and lead-induced oxidative damage in lead-exposed mice; the result may provide a theoretical reference for the treatment of Pb poisoning.

A Review on Coordination Properties of Thiol-Containing Chelating Agents Towards Mercury, Cadmium, and Lead.

The present article reviews the clinical use of thiol-based metal chelators in intoxications and overexposure with mercury (Hg), cadmium (Cd), and lead (Pb). Currently, very few commercially available pharmaceuticals can successfully reduce or prevent the toxicity of these metals. The metal chelator meso-2,3-dimercaptosuccinic acid (DMSA) is considerably less toxic than the classical agent British anti-Lewisite (BAL, 2,3-dimercaptopropanol) and is the recommended agent in poisonings with Pb and organic Hg. Its toxicity is also lower than that of DMPS (dimercaptopropane sulfonate), although DMPS is the recommended agent in acute poisonings with Hg salts. It is suggested that intracellular Cd deposits and cerebral deposits of inorganic Hg, to some extent, can be mobilized by a combination of antidotes, but clinical experience with such combinations are lacking. Alpha-lipoic acid (α-LA) has been suggested for toxic metal detoxification but is not considered a drug of choice in clinical practice. The molecular mechanisms and chemical equilibria of complex formation of the chelators with the metal ions Hg2+, Cd2+, and Pb2+ are reviewed since insight into these reactions can provide a basis for further development of therapeutics.

Allicin alleviated learning and memory deficits caused by lead exposure at developmental stage.

AIMS: It is a promising approach to search the therapeutic strategies for treating lead (Pb) toxicity. Allicin, a natural compound extracted from Allium sativum (garlic), has been reported to have many beneficially biological properties. In this study, we investigated the protective effects of allicin on learning and memory function of rats exposed by lead acetate at developmental stage. MATERIALS AND METHODS: Rats received lead acetate for inducing toxicity, and gavaged with allicin to ameliorate this toxicity. Morris water maze test was performed to determine learning and memory function. Superoxide dismutase (SOD), glutathione (GSH) and methane dicarboxylic aldehyde (MDA) was measured to determine oxidative stress. Immunofluorescence was carried out to analyze GFAP-positive cells. The protein expression of ERK, p-ERK, EGFR and p-EGFR were detected using western blot. KEY FINDINGS: We found that allicin ameliorated lead acetate-caused learning and memory deficits by promoting hippocampus astrocyte differentiation, which mainly through EGFR/ERK signaling. Moreover, allicin attenuated the increased ROS level by regulating the oxidative defense system. SIGNIFICANCE: These results suggest that allicin is a potent agent able to ameliorate lead acetate-induced learning and memory deficits during early development, and may thus be useful for defeating lead acetate toxicity.

Protective effects of a Lachnum polysaccharide against liver and kidney injury induced by lead exposure in mice.

This study was designed to investigate the liver and kidney protective efficacy of a Lachnum polysaccharide (LEP) against Pb-induced toxicity in mice. The results showed that LEP decreased the Pb-induced bodyweight loss and organ index. Moreover, biochemical analysis showed that treatment of LEP could improve antioxidant status (CAT, GSH-Px and MDA) and the injury of tissues (liver and kidney). In addition, the histopathological observations indicated that LEP could attenuate liver and kidney cell injury induced by Pb. For further studies, key proteins involved in hepatic and kidney apoptosis, including cleaved caspase-3, Bax, Bcl-2, TGF-ß1 and α-SMA, were quantified. The present findings demonstrated that LEP is strongly effective in protecting against the liver and kidney injury induced by Pb. We hope this research can offer a theoretical base for development of polysaccharide based on nutraceutical food in future.

CHOP/caspase-3 signal pathway involves in mitigative effect of selenium on lead-induced apoptosis via endoplasmic reticulum pathway in chicken testes.

Lead (Pb) is an environmental pollutant. Selenium (Se) has alleviative effect on Pb poisoning. However, mitigative effect of Se on Pb-induced apoptosis has not been unclear via endoplasmic reticulum (ER) pathway in chicken testes. The aim of this study was to investigate mitigative effect of Se on apoptosis induced by Pb poisoning via ER pathway in chicken testes. Sixty male chickens (7-day-old) were randomly divided into the control group offered drinking water (DW) and basic diet (BD) (0.49 mg/kg Se), the Se group offered DW and BD containing Na2SeO3 (SeBD) (1.00 mg/kg Se), the Pb group offered DW containing (CH3OO)2Pb (PbDW) (350.00 mg/L Pb) and BD, and the Pb + Se group offered PbDW and SeBD; and were fed for 90 days. The following contents were performed as follows: histology; antioxidant indexes (reduced glutathione (GSH), malondialdehyde (MDA), glutathione peroxidase (GPx), glutathione S-transferase (GST), and superoxide dismutase (SOD)); mRNA expressions of ER-related genes (glucose-related protein 78 (GRP78), protein kinase-like ER kinase (PERK), eukaryotic initiation factor 2α (eIF2α), activating transcription factor 4 (ATF4), and enhancer-binding protein homologous protein (CHOP)); and apoptosis-related genes (cysteine-aspartic protease (caspase)-3 and caspase-12) in chicken testes. The results indicated that Pb poisoning caused histological changes; increased MDA content; decreased the content of GSH and the activities of GPx, GST, and SOD; and upregulated mRNA expressions of the above five ER-related genes and two apoptosis-related genes in the chicken testes. Se alleviated Pb-induced oxidative stress, ER stress, and apoptosis via CHOP/caspase-3 signal pathway in the chicken testes.

Elevated lead level from a tobacco source requiring chelation in a 12-year-old child.

CONTEXT: Across the world, tobacco is used in a variety of forms, including being smoked or added to a "quid" that is then chewed. We report a case of lead poisoning in a child from tobacco imported from Thailand. CASE DETAILS: A 12-year-old Thai immigrant boy had a blood lead level (BLL) of 6 mcg/dL on routine testing upon arrival to the United States, but which increased to 72 mcg/dL six months after his arrival. He was asymptomatic with unremarkable workup. At this time his father, mother and two siblings were also found to have elevated BLLs of 53, 16, 22, and 11 mcg/dL, respectively. Water, paint, food and cookware sources tested negative for lead, whereas samples of the father's dried tobacco leaves imported from Thailand contained 36.12 ppm (mcg/g) of lead. The mother admitted that both she and the patient used the tobacco as well. The child was chelated with oral succimer and his BLL decreased. DISCUSSION: In our case, the source of the lead exposure was from the tobacco that the patient was chewing. Tobacco is often overlooked as a source of lead exposure, though it has been reported in the literature, both from direct smoking and from chewing, as well as through secondhand smoke. Toxicologists and health care professionals should consider cultural practices when evaluating patients with elevated BLLs.

Proanthocyanidins Attenuation of Chronic Lead-Induced Liver Oxidative Damage in Kunming Mice via the Nrf2/ARE Pathway.

Lead is harmful for human health and animals. Proanthocyanidins (PCs), a natural antioxidant, possess a broad spectrum of pharmacological and medicinal properties. However, its protective effects against lead-induced liver damage have not been clarified. This study was aimed to evaluate the protective effect of PCs on the hepatotoxicity of male Kunming mice induced by chronic lead exposure. A total of 70 healthy male Kunming mice were averagely divided into four groups: control group, i.e., the group exposed to lead, the group treated with PCs, and the group co-treated with lead and PCs. The mice exposed to lead were given water containing 0.2% lead acetate. Mice treated in the PCs and PCs lead co-treated groups were given PC (100 mg/kg) in 0.9% saline by oral gavage. Lead exposure caused a significant elevation in the liver function parameters, lead level, lipid peroxidation, and inhibition of antioxidant enzyme activities. The induction of oxidative stress and histological alterations in the liver were minimized by co-treatment with PCs. Meanwhile, the number of Transferase-Mediated Deoxyuridine Triphosphate-Biotin Nick End Labeling (TUNEL)-positive cells was significantly reduced in the PCs/lead co-treated group compared to the lead group. In addition, the lead group showed an increase in the expression level of Bax, while the expression of Bcl-2 was decreased. Furthermore, the lead group showed an increase in the expression level of endoplasmic reticulum (ER) stress-related genes and protein (GRP78 and CHOP). Co-treated with PCs significantly reversed these expressions in the liver. PCs were, therefore, demonstrated to have protective, antioxidant, and anti-ER stress and anti-apoptotic activities in liver damage caused by chronic lead exposure in the Kunming mouse. This may be due to the ability of PCs to enhance the ability of liver tissue to protect against oxidative stress via the Nrf2/ARE signaling pathway, resulting in decreasing ER stress and apoptosis of liver tissue.

Heavy Metal-Induced Systemic Dysfunction Attenuated by Tannic Acid.

Lead toxicity is a major public health concern. This study was designed to investigate the effects of oral administration of tannic acid (TA) on lead acetate (LA)-induced oxidative stress in rat liver and kidney. Rats were treated with 50 mg/kg body weight of TA against LA-induced oxidative stress 3 times/week for 2 weeks. At a rate of 50 mg/kg of body weight, LA was given intraperitoneally 3 times/week for 2 weeks. Results show significantly elevated levels of oxidative stress markers observed in LA-treated rats, whereas significant depletion in the activity of nonenzymatic and enzymatic antioxidants as well as histological changes were observed in LA-treated rat liver and kidney. TA treatment significantly attenuated the altered levels of oxidative stress biomarkers for nonenzymatic and enzymatic antioxidants. We demonstrated that TA exhibits potent antioxidant and protected against oxidative damage in rat liver and kidney induced by LA treatment. These findings were further supported by histopathological findings in liver and kidney showing that TA protected tissue from the deleterious effects of LA treatment. These outcomes suggest that the consumption of TA may confer a protective effect against lead intoxication through its antioxidative effect.