Showing papers on "Lead acetate published in 2012"

Effect of lead acetate toxicity on experimental male albino rat

Abstract: Objective To evaluate the effect of different doses of lead acetate (1/20, 1/40 and 1/60 of LD50) on body weight gain, blood picture, plasma protein profile and the function of liver, kidney and thyroid gland.

Protective Effect of Naringenin Against Lead-Induced Oxidative Stress in Rats

Abstract: Oxidative stress is thought to be involved in lead-induced toxicity. The aim of this study was to investigate the possible protective role of naringenin on lead-induced oxidative stress in the liver and kidney of rats. In the present investigation, lead acetate (500 mg Pb/L) was administered orally for 8 weeks to induce hepatotoxicity and nephrotoxicity. The levels of hepatic and renal markers such as alanine aminotransferase, aspartate aminotransferase, urea, uric acid, and creatinine were significantly (P < 0.05) increased following lead acetate administration. Lead-induced oxidative stress in liver and kidney tissue was indicated by a significant (P < 0.05) increase in the level of maleic dialdehyde and decreased levels of reduced glutathione, superoxide dismutase, catalase, and glutathione peroxidase. Naringenin markedly attenuated lead-induced biochemical alterations in serum, liver, and kidney tissues (P < 0.05). The present study suggests that naringenin shows antioxidant activity and plays a protective role against lead-induced oxidative damage in the liver and kidney of rats.

Lactobacillus plantarum CCFM8661 alleviates lead toxicity in mice.

Abstract: Lead causes a broad range of adverse effects in humans and animals. The objective was to evaluate the potency of lactobacilli to bind lead in vitro and the protective effects of a selected Lactobacillus plantarum CCFM8661 against lead-induced toxicity in mice. Nine strains of bacteria were used to investigate their binding abilities of lead in vitro, and L. plantarum CCFM8661 was selected for animal experiments because of its excellent lead binding capacity. Both living and dead L. plantarum CCFM8661 were used to treat 90 male Kunming mice during or after the exposure to 1 g/L lead acetate in drinking water. The results showed oral administration of both living and dead L. plantarum CCFM8661 offered a significant protective effect against lead toxicity by recovering blood δ-aminolevulinic acid dehydratase activity, decreasing the lead levels in blood and tissues, and preventing alterations in the levels of glutathione, glutathione peroxidase, malondialdehyde, superoxide dismutase, and reactive oxygen species caused by lead exposure. Moreover, L. plantarum CCFM8661 was more effective when administered consistently during the entire lead exposure, not after the exposure. Our results suggest that L. plantarum CCFM8661 has the potency to provide a dietary strategy against lead toxicity.

The protective effect of green tea extract on lead induced oxidative and DNA damage on rat brain.

Abstract: The role of green tea in protection against neurotoxicity induced by lead acetate was investigated in rats. Five equal groups, each of ten rats were used. The first group was served as control, the second, third, and fourth groups were given lead acetate, lead acetate and green tea, and green tea only, respectively, for one month, the fifth group was administered lead acetate for one month followed by green tea for 15 days. Lead acetate was given orally at a dose of 100 mg/kg b. wt, while green tea was given in drinking water at a concentration of 5 g/L. Lead acetate administration induced loss of body weight and decreased concentration of reduced glutathione and SOD activity in brain tissues as well as significantly high DNA fragmentation and pathological changes. Co-administration of green tea with lead acetate significantly alleviated these adverse effects.

Flaxseed Oil as a Neuroprotective Agent on Lead Acetate-Induced Monoamineric Alterations and Neurotoxicity in Rats

Abstract: Lead remains a considerable occupational and public health problem, which is known to cause a number of adverse effects in both man and animals. Here, the neuroprotective effect of flaxseed oil (1,000 mg/kg) on lead acetate (20 mg/kg) induced alternation in monoamines and brain oxidative stress was examined in rats. The levels of lead, dopamine (DA), norepinephrine (NE), serotonin (5-HT), lipid peroxidation, nitrite/nitrate (NO), and glutathione (GSH) were determined; also, the activity of acetylcholinesterase (AChE) and Na+-K+-ATPase were estimated on different brain regions of adult male albino rats. The level of lead was markedly elevated in different brain regions of rats. This leads to enhancement of lipid peroxidation and NO production in brain with concomitant reduction in AChE activity and GSH level. In addition, the levels of DA, NE, and 5-HT were decreased in the brain. These findings were associated with BAX over expression. Treatment of rats with flaxseed oil induced a marked improvement in most of the studied parameters as well as the immunohistochemistry features. These data indicated that dietary flaxseed oil provide protection against lead-induced oxidative stress and neurotoxic effects.

Antioxidant and Tissue-Protective Studies on Ajwa Extract: Dates from Al-Madinah Al-Monwarah, Saudia Arabia

Abstract: The objective was to study the in-vivo protective effect of Al-Madinah Ajwa (name of the most famous date in Al-Madinah Al-Monwarah City) extract against lead acetate toxicity on the tissues of vital organs. Four rabbit groups were used as an animal model for this study. Ajwa extract treated group (300 mg/kg/day, for 14 days) were evaluated for lead acetate (500 ppm in drinking water for 14 days) intoxication compared to lead acetate alone-intoxicated group; Ajwa extract group and control group. This was done by assessment of liver and kidney functions, blood lead levels, levels of oxidants-antioxidants and histopathological changes in liver, kidney, heart and lung in different groups. The lead acetate intoxicated group showed significant elevation of serum glutamic pyruvic transaminase (SGPT), serum glutamic oxaloacetic transaminase (SGOT), alkaline phosphatase (ALP), total bilirubin (TB), serum creatinine-urea (Cr-U), lipid hydroperoxide (LPO), protein carbonyl content (PCC), and depression of Superoxide dismutase (SOD) and Glutathione peroxidase (GPX) levels as compared to control. The Agwa extract showed tissue protective effect by significant restoration of (SGPT), (SGOT), (ALP), (TB), (Cr-U) (LPO), (PCC), (SOD) and (GPX) levels compared to the previous group. The histopathological evaluation showed marked vascular congestion, interstitial hemorrhage, cellular degeneration and necrosis in different organs of lead acetate intoxicated group, while Agwa extract treated group showed mild congestion and slight focal cellular degeneration. Therefore, outcome of the present study validates the ameliorative and protective effects of Al-Madinah Ajwa dates against the toxic effects of lead acetate poisoning.

Oxidative stress: a possible mechanism for lead-induced apoptosis and nephrotoxicity

Abstract: Lead-induced nephrotoxicity is a human health hazard problem. In this study, Human mesangial cells (HMCs) were treated with different concentration of lead acetate (5, 10, 20 μmol/l) in order to investigate the oxidative stress and apoptotic changes. It was revealed that lead acetate could induce a progressive loss in HMCs viability together with a significant increase in the number of apoptotic cells using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl tetrazolium (MTT) assay and flow cytometry, respectively. The apoptotic morphological changes induced by lead exposure in HMCs were demonstrated by PI-Hochest33342 staining. A DNA laddering pattern in lead-treated cells was shown, which could indicate nuclear fragmentation. In addition, lead acetate significantly increased the levels of malondialehyde (MDA) content and lactate dehydrogenase (LDH) activity. Therefore, it might be concluded that lead could promote HMCs’ oxidative stress and apoptosis, which may be the chief mechanisms of lead-induced nephrotoxicity.

Oxidative damage and OGG1 expression induced by a combined effect of titanium dioxide nanoparticles and lead acetate in human hepatocytes

Abstract: Titanium dioxide (TiO2) is a widely used nanomaterial that can cause biological damage through oxidative stress. At low concentrations, TiO2 can interact with lead acetate (PbAc) to produce different toxic responses, compared with TiO2 or PbAc alone. In this study, we utilized the following as indicators of toxic responses in human embryo hepatocytes (L02): reactive oxygen species (ROS), reduced glutathione (GSH), superoxide dismutase (SOD), and the DNA adducts 8-hydroxydeoxyguanosine (8-OHdG) and 8-oxoguanine DNA glycosylase homolog 1 (OGG1). These were used to evaluate the oxidative stress of TiO2 (at 0.001, 0.01, 0.1, 1, and 10 μg mL−1) mixed with PbAc (1 μg mL−1) on L02 cells without photoactivation. Compared with the negative control (1‰ dimethyl sulfoxide), TiO2 mixed with PbAc induced increased release of ROS (at 0.001, 0.01, 0.1, 1, 10 μg mL−1 TiO2), intracellular SOD activity (at 0.1 and 0.01 μg mL−1 TiO2), GSH levels (at 0.01–1 μg mL−1 TiO2), 8-OHdG levels (at 1 and 10 μg mL−1 TiO2), OGG1 expression (at 0.001–1 μg mL−1 TiO2), and cytotoxicity (at 0.1, 1, and 10 μg mL−1 TiO2) in L02 cells. There were no significant changes in ROS, GSH, SOD, 8-OHdG, or OGG1 levels when L02 cells were treated with TiO2 alone or PbAc alone. These findings indicate that TiO2 and PbAc in combination induce cytotoxicity and oxidative stress in L02 cells in the absence of photoactivation. © 2011 Wiley Periodicals, Inc. Environ Toxicol, 2012.

Effects of Lead Exposure on DNA Damage and Apoptosis in Reproductive and Vital Organs in Female Rabbits

Abstract: The aim of the present study was to investigate the toxic effect of prolonged lead exposure on DNA damage and tissue apoptosis of female rabbits. Thirty mature female New Zealand rabbits were used in three groups, each of ten animals. The first group served as a control, the second group (low dose group) and the third group (high dose group) were given lead acetate at a dose of 15 mg/kg and 30mg/kg respectively. Lead acetate was given by oral route for 8 weeks (five days a week). By the end of the experiment, tissue samples were collected for DNA extraction and pathological examination of the reproductive and vital organs. Results revealed that lead induced cellular DNA damage and tissue apoptosis. Pathological examination of the ovarian tissues showed diffused atretic and degenerative changes of growing and mature follicles. Diffused apoptosis of the epithelial lining of the endometrial and uterine glands were seen. Degeneration and focal necrosis in the vital organs as liver, heart, kidney and brain were noticed. Infarction of the kidneys was detected at high dose group. Intranuclear specific inclusion bodies in liver and kidney tissues were detected. In conclusion, lead acetate has a direct effect on DNA causing damage and apoptosis in tissue of female rabbit and may contribute in reduction of fertility. Also chronic lead toxicity is responsible for hepatic, myocardium, nervous pathological changes and renal failure of rabbits.

Differential effect of postnatal lead exposure on gene expression in the hippocampus and frontal cortex

Abstract: Although developmental lead exposure is known to have detrimental effects on a variety of cognitive functions that depend on the integrity of the hippocampus and frontal cortex, little is known about how low levels of lead exposure affect expression of key families of genes in these structures. The present study examined the effects of exposure to environmentally relevant levels of lead during the sensitive early post-weaning period in the rat on the expression profiles of a select number of neurobiologically relevant genes (i.e., genes for neurotrophic factors, NMDA receptors, metabotropic glutamate receptors, synaptic function/plasticity, cell signaling, and transcription/regulation) in the rat hippocampus and frontal cortex. Exposure to lead (180 and 375-ppm lead acetate in food for 30 days) significantly increased blood lead levels (5.8 to 10.3 μg/dl) and significantly affected expression of many of the genes examined. In many instances, lead exposure had different effects on the same gene depending on the brain region in which the expression of that gene was examined. Gene expression in the frontal cortex was often more sensitive to modification than gene expression in the hippocampus. These results suggest that even past infancy, exposures to low levels of lead can have significant effects on gene expression in the frontal cortex and the hippocampus with the potential to exert long-term effects on behavior and cognition.

PROTECTIVE EFFECT OF AQUEOUS LEAF EXTRACT OF Murraya koenigi AGAINST LEAD INDUCED OXIDATIVE STRESS IN RAT LIVER, HEART AND KIDNEY: A DOSE RESPONSE STUDY

Abstract: The current studies evaluated whether an aqueous extract of the leaves of Murraya Koenigii (Curry leaves) has the ability to protect against lead – induced oxidative stress in the liver, heart and kidneys of experimental rats. The studies revealed that the extract dose dependently protected the biomarkers of tissue damage, oxidative stress and antioxidant enzymes from getting altered in the rat tissues following treatment with lead acetate. The results indicate that the aqueous curry leaf extract (CuLE) might have protected the rat tissues from lead acetate induced oxidative stress through antioxidant mechanism(s).As curry leaves form one of the important component of regular diet.

Oral administration of vitamin C and vitamin E ameliorates lead-induced hepatotoxicity and oxidative stress in the rat brain.

Abstract: Background: Lead toxicity is a public health concern. Lead is one of the dispensable and non-biodegradable heavy metals and is toxic even at low concentrations. Objective: This study was to investigate the effect of oral administration of Vitamin C and Vitamin E on lead-induced hepatotoxicity and oxidative stress in the brain of rats. Methods : Thirty Sprague-Dawley albino male albino rats (115.58 ± 4.96g) were divided equally into five groups. The rats were fed rat chow and water ad libitum. Group 1 rats served as control and were orally administered 2ml saline every day for 7 weeks. Group 2 rats received orally 2ml lead acetate solution (60mg/kg body weight) every day for 7 weeks. Group3 rats received orally 2ml lead acetate solution (60mg/kg body weight) and vitamin C (40mg/kg body weight) every other day for 7 weeks. Group 4 rats received orally 2ml lead acetate solution (60mg/kg body weight) and vitamin E (150mg/kg body weight)every day for 7weeks. Group 5 received orally lead acetate solution at 60mg/kg body weight and vitamin C (40mg/kg body weight)and vitamin E (150mg/kg body weight) every other day for 7weeks. Three rats from each group were sacrificed after the fourth week. The remaining rats were sacrificed after the seventh week. Changes in body weight, liver weight, brain weight, activities of liver function enzymes (aspartate amino transferase (AST), alanine amino transferase (ALT) and alkaline phosphatase(ALP) in the serum at week 4 and week 7 were assayed.The oxidative stress markers (reduced glutathione (GSH), nitric oxide(NO), malondialdehyde(MDA), levels, catalase(CAT) and superoxide dismutase (SOD) activities) were determined in the brain of rats. Serum lead level of rats was also determined. Results: The lead Pb exposed rats caused a significant (p<0.01) increase in bioavailable lead in the blood (p<0.05) as compared to the control. AST, ALT and ALPactivities were significantly increased (p<0.05) in the serum of rats exposed to lead as compared to the control. NO and MDA levels were significantly increased (p<0.05) in the brain of rats exposed to lead, while GSH level, SOD and CAT activities were significantly reduced (p<0.05) in the brain of rats exposed to lead when compared with the control. Conclusion : Data of the study indicate that oral administration of vitamin C and vitamin E significantly reduced the blood lead concentration, ameliorates the hepatic damage and significantly reduced the oxidative stress in the brain of rats. Key Words : Lead-induced hepatotoxicity, oxidative stress, vitamins C& E, rat brain

Neurochemical and Neurobehavioral Effects of Low Lead Exposure on the Developing Brain

Abstract: Lead is found in small but appreciable quantities in air, soil drinking water and food. Exposure to such amounts of lead does not cause acute lead toxicity, but produces subtle effects, particularly in children. The CDC advocates “safe” or “acceptable” levels of blood lead up to 10 μg/dl, while OSHA declares blood lead levels up to 40 μg/dl as “safe” or “acceptable” in the occupationally exposed. The objective of the study was to see if blood levels considered “safe” can cause changes in the biogenic neurotransmitters in the developing brain which may cause neurobehavioral defects like hyperactivity and other cognitive disorders. Albino Wistar rats were divided into the control and lead-treated groups. The control group was given unleaded water, while the lead-treated group was fed with 50 ppm lead acetate in drinking water. On day 45 the animals were subjected to a passive avoidance test, their blood analysed for ZPP and lead. They were then sacrificed and the neurotransmitters—Norepinephrine (NE) and its metabolite—methoxyhydroxyphenylglycol (MHPG) estimated in the brain areas associated with learning and memory—the frontal cortex, hippocampus and the striatum by HPLC-ECD. Our results showed significant increases in blood lead, NE and MHPG, while ZPP increase was insignificant. The rats showed neurobehavioral abnormalities as assessed by the passive avoidance test. We concluded that low blood levels of lead cannot be considered “safe” or “acceptable” as it causes neurotransmitter alterations. Increased NE turnover is implicated in hyperactivity disorders such as ADHD and Tourette syndrome.

Grape Seed Extract (Vitisvinifera) Alleviate Neurotoxicity and Hepatotoxicity Induced by Lead Acetate in Male Albino Rats

Abstract: Grape seed extracts (GSE) are very potent antioxidant and exhibit numerous interesting pharmacologic activities, including an antioxidant property, and has been suggested to be of use in treatment of several diseases. The present study has been undertaken to investigate the protective and therapeutic effect of GSE against lead-induced neuro and hepatotoxicity in rat. Male albino rats were divided into six groups: the 1st group, rats were injected daily with saline vehicle and served as negative control, the 2nd group (positive control group), the rats were injected (i.p.) with subacute dose (100 mg/kg b·w/day) of lead acetate (LA). The 3rd group (protective group), the rats were injected (i.p.) with LA (100 mg/kg b·w/day) for 7 days after treatment with GSE (100 mg/kg b·w/day) for 3 weeks. The 4th, 5th and 6th groups (therapeutics groups), rats were injected (i.p.) with subacut dose (100 mg/kg b·w/day) of lead acetate for 7 days, then treated with GSE (100 mg/kg b·w/day) for one, two and three weeks, respectively. The level of norepinephrine (NE), dopamine (DA), serotonin (5-HT) and 5-hydroxyindol acetic acid (5-HIAA) were evaluated in brain regions (cerebellum, brainstem, striatum, cerebral cortex, hypothalamus and hippocampus). The result indicated that the administration of subacute dose of LA (100 mg/kg/day, i.p.) induce a significant decrease in NE, DA, 5-HT and 5-HIAA content in all tested brain regions. Also the obtained data showed significant increase in liver enzymes: serum glutamate oxaloacetate transaminase (GOT), serum glutamate pyruvate transaminase (GPT) and Lactate dehydrogenase (LDH) level in group 2 (positive control). There is an improvement in neurotransmitters content. Also the obtained data showed significant in- crease in liver enzymes of protective (G3) and therapeutics groups (G4, G5 and G6) which received GSE compared with animal group that received lead acetate (G2). This is may be the presence of proanthocyanidins and procyanidins which have antioxidant and free radical scavenging activities. The result suggests that grape seed extract may prevent lead-induced neurotoxicity and hepatotoxicity.

Biochemical and reproductive effects of gestational/lactational exposure to lead and cadmium with respect to testicular steroidogenesis, antioxidant system, endogenous sex steroid and cauda‐epididymal functions

Abstract: This study investigated the effects of gestational and lactational exposure to lead and cadmium on testicular steroidogenesis, antioxidant system and male accessory gland functions in F1 generation rats to understand the biochemical mechanisms involved in endocrine disruptions. Pregnant rats were subcutaneously administered with 0.05 mg kg(-1) body wt\ day(-1) of sodium acetate (control), lead acetate, cadmium acetate and (lead acetate + cadmium acetate) throughout the gestational-lactational period, and all animals from each of the experimental groups were sacrificed by decapitation on post-natal day 56 for performing various biochemical assays. We observed significant reduction in the activities of testicular key steroidogenic enzymes and serum testosterone concentration along with significant depletion in cholesterol, ascorbic acid and reduced glutathione contents in all the metal-treated groups. Reductions in the activities of catalase and superoxide dismutase with concomitant increase in the levels of thiobarbituric acid reactive substance were observed in experimental groups. Both sperm contents and sperm motility patterns were significantly altered in all the metal-treated groups, suggesting the direct/indirect spermotoxic effects of lead and cadmium. The inhibitory effects of lead, cadmium and combined exposure on testicular steroidogenesis machinery, along with the male accessory gland functions, are indicative of multiple targets of lead and cadmium to disrupt male reproductive functions.

Effect of Lead Toxicity on Cytogenisity, Biochemical Constituents and Tissue Residue with Protective Role of Activated Charcoal and Casein in Male Rats

Abstract: Lead is a common industrial and environmental pollutant. Prolonged exposure of a sub- lethal dose to this toxicant is associated with oxidative stress, damage of DNA and considered to be a risk factor for kidney, liver added to many disorders. This study was carried out to investigate the most toxic effects of lead with trial to diminish this toxicity by supplementation of casein or activated charcoal. Therefore, forty mature male albino rats were used , they divided into four equal groups, 10 rats of each. Group 1 was considered as control. Rats of other groups (2, 3 and 4) were supplemented lead acetate at a dose of 0.5 g/100 ml drinking water for 2 months. Gr 3 is given charcoal at a concentration of 0.05g ration, while in Gr 4 casein is mixed with ration at a concentration of 20 g/100 g ration. Group 2 revealed significant increases in serum AST, ALT, ALP, LDH, GGT, TB, TC, LDL and CAT levels and decreased total protein, HLDL, VLDL, trace mineral salts, SOD and GSH- px. The results of haematological study evoked a significant decrease in the red blood cells (RBCs) count, blood haemoglobin (Hb) concentration and packed cell volume (PCV). Cytogenetic study resulted a significant increase in the percent of multinucleated polychromatic erythrocytes (MPCE) as well as significant increase in the polychromatic- erythrocytes (PCE) and normochromatic erythrocyte (NCE) ratio (PCER/NCE) Lead concentration in level serum and different tissues showed lead accumulation in serum, kidney, liver, muscle, intestine and spleen. Supplementation of charcoal and casein induce protective effects against lead toxicity in most of above parameter studies, and casein showed higher efficacy in the protection of lead- induced toxicity than charcoal.

Effect of melatonin administration on DNA damage and repair responses in lymphocytes of rats subchronically exposed to lead.

Abstract: Lead exposure induces DNA damage, oxidative stress, and apoptosis, and alters DNA repair. We investigated the effects of melatonin co-administered to rats during exposure to lead. Three doses of lead acetate (10, 50 and 100 mg/kg/day) were administered to rats during a 6-week period. Lymphocytes were analyzed. Lead exposure decreased glutathione (GSH) levels in blood, and at doses of 100 mg/kg/day and 50 mg/kg/day without melatonin, caused high levels of DNA damage, induced apoptosis, and altered DNA repair. Melatonin co-treatment did not attenuate the effects of lead at 100 mg/kg/day, indicating that the effect of melatonin on GSH reduction is not sufficient to reduce the genotoxic effects of lead at this high dose. After 6 weeks of treatment, decreased weight gain was observed in high lead-dose groups (100 mg/kg/day), with or without melatonin, and in medium-dose groups (50 mg/kg/day) with melatonin, compared with the control group. The protective action of melatonin against lead toxicity is dependent on the dose of lead. Further pharmacological studies are needed to determine whether melatonin acts via melatonin membrane receptors on lymphocytes.

Early postnatal lead exposure induces tau phosphorylation in the brain of young rats.

Abstract: Cognitive impairment is a common feature of both lead exposure and hyperphosphorylation of tau. We, therefore, investigated whether lead exposure would induce tau hyperphosphorylation. Wistar rat pups were exposed to 0.2% lead acetate via their dams’ drinking water from postnatal day 1 to 21. Lead in blood and brain were measured by atomic absorption spectrophotometry and the expression of tau, phosphorylated tau and various serine/threonine protein phosphatases (PP1, PP2A, PP2B and PP5) in the brain was analyzed by Western blot. Lead exposure significantly impaired learning and resulted in a significant reduction in the expression of tau but increased the phosphorylation of tau at Ser199/202, Thr212/Ser214 and Thr231. PP2A expression decreased, whereas, PP1 and PP5 expression increased in lead-exposed rats. These results demonstrate that early postnatal exposure to lead decrease PP2A expression and induce tau hyperphosphorylation at several serine and threonine residues. Hyperphosphorylation of tau may b...

Protective Effects of Latex of Ficus carica L. against Lead Acetate-Induced Hepatotoxicity in Rats

Abstract: Ficus carica L. latex is used traditionally for many therapeutic purposes. Oxidative stress may be the main reason behind most histological and cellular effects of lead. The aim of this study was to investigate the possible hepatoprotective role of Ficus carica L .latex against lead acetate-induced oxidative stress in rats. In the present investigation, lead acetate (500 mg Pb/L) was given orally to male rats for 28 days to induce hepatotoxicity. The Ficus latex was found to contain high total phenols and flavonoids. The levels of hepatic markers such as alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP) were significantly (P�<�0.05) increased in blood serum following lead acetate administration. Lead-induced oxidative stress in liver tissue was indicated by a significant (P�<�0.05) increase in the level of liver Malondialdehyde (MDA) and decreased levels of liver reduced glutathione (GSH) and superoxide dismutase (SOD). Histologically and ultrastructurally, the liver showed several histological alterations such as degeneration of hepatocytes by necrosis and apoptosis, fatty changes and inflammatory cells infiltration. Ficus latex (1mL of 1:50 diluted latex/kg b.wt) markedly attenuated the previous lead-induced biochemical alterations in serum and liver tissues (P�<�0.05) as well as the histological and cellular changes. From this study, it can be concluded that the Ficus latex showed effective hepatoprotective and antioxidative action against lead acetate-induced hepatotoxicity in rats.