Immunoprotective effect of curcumin on cypermethrin-induced toxicity in rats

Immunotoxicological effects of cypermethrin and their reversal by curcumin following oral administration were evaluated in rats. Mature male Wistar rats were orally administered cypermethrin (25?mg?kg^?1 body wt), curcumin (100?mg?kg^?1 body wt) or both daily for 4 weeks. At the end of fourth week, hematological, serum biochemical, and immunological parameters were studied. Subchronic exposure to cypermethrin significantly reduced body weight, total leukocyte count, lymphocyte count, serum total protein, serum albumin, serum globulin, antibody titer against sheep red blood cells, and cell-mediated immunity. Concomitant curcumin administration restored the changes in the body weight, hematological parameters, and serum biochemical indices and significantly increased the antibody titer, and cell mediated immunity. These results suggest that concurrent curcumin treatment has a beneficial role in mitigating immunotoxicological and other adverse effects of cypermethrin.     

Protective efficacy of Mucuna pruriens extract on Epichlorohydrin induced toxicity in epididymis of albino rats

The protective effects of seeds of Mucuna pruriens on epichlorohydrin (ECH)-induced toxicity in epididymis and epididymal sperms of rats were studied. Different doses of ECH and M. pruriens (75 and 100 mg kg^?1, respectively) were administered daily, orally for 70 days. Group I animals served as control. Group II and III rats received ECH (75 or 100 mg kg^?1 body weight, respectively) alone. The group IV and V rats received a combination of both ECH and the seed extract of M. pruriens at 75 or 100 mg kg^?1 body weight. Group VI rats was administered only the extract of M. pruriens 100 mg kg^?1 body weight. At the end of the experiment (71st day), rats were sacrificed and sperm collected from epididymis were used for the assessment of sperm count, sperm viability, and sperm motility. Administration of ECH produced a reduction in epididymal sperm count, sperm viability, and sperm motility. The activities of catalase, superoxide dismutase, and glutathione peroxidase were decreased, while lipid peroxidation was increased. ECH produced a decrease in the levels of protein, acid phosphatase, sialic acids, and increased the level of alkaline phosphatase, and cholesterol. The administration of M. pruriens to ECH-treated rats resulted in a protective effect.     

Evaluation of vitamin E and calcium effects on fluoride toxicity-induced fertility impairment

Chronic fluoride (Fl) toxicity is a serious public health problem globally where drinking water contains more than 1 ppm of Fl. Sodium fluoride (NaF) produced male reproductive system toxicity. The aim of the present study was to evaluate the amelioration of Fl toxicity-induced fertility impairment by vitamin E and calcium during the withdrawal period. The study was carried out on 70 adult male albino rats divided into five main groups: group I control; subdivided into group Ia (maintained on standard diet and water ad libitum for 60 days) and group Ib (maintained on standard diet and water ad libitum for 120 days), group II was administered NaF and subdivided into group IIa (administered NaF for 60 day and sacrificed) and group IIb (administered NaF for 60 day then maintained on standard diet and water ad libitum for a further 60 days), and treated groups III, IV, and V were administered NaF. Rats were maintained during withdrawal from NaF, on vitamin E (10 mg kg^?1 day^?1 for 60 days), calcium (50 mg kg^?1 day^?1 orally for 60 days), and both vitamin E and calcium, respectively. The duration of NaF administration was 60 days at a dose 20 mg kg^?1 day^?1 for all treated groups. The following parameters were determined: body and organ weights, sperm motility, sperm morphology, sperm viability, fertility test, and hormone assays: testosterone, in vitro testosterone production, luteinizing hormone, and follicular stimulating hormone. The combined administration of vitamin E and calcium during withdrawal from NaF showed significant improvement from chronic FL-induced toxicity on male reproductive organs.     

Sensorimotor performance deficits induced by chronic chlorpyrifos exposure in Wistar rats: mitigative effect of vitamin C

This study was aimed at evaluating the ameliorative effect of vitamin C on chlorpyrifos-induced sensorimotor changes involving postural reflex, limb placing, and vibrissae touch in Wistar rats. Forty adult Wistar rats of either sex were divided into 4 groups of 10 animals in each group. Group I was administered soya oil (2?mL?kg^?1) while group II was given vitamin C (100?mg?kg^?1); group III was dosed with chlorpyrifos (10.6?mg?kg^?1, i.e. ～1/8th of the LD₅₀); group IV was administered vitamin C (100?mg?kg^?1) and then exposed to chlorpyrifos (10.6?mg?kg^?1), 30?min later. The regimens were administered by gavage once daily for a period of 17 weeks. Neurobehavioral parameters involving postural reflex, limb placing, and vibrissae touch responses measured at various intervals revealed a deficit in postural reflex, limb placing, and vibrissae touch responses in the CPF group, which was mitigated by vitamin C pretreatment. The neuronal and glial cell degeneration, increased brain malonaldehyde concentration, and decrease in superoxide dismutase, catalase, and acetylcholinesterase activities recorded in the group given chlorpyrifos were ameliorated by vitamin C. Therefore, vitamin C was shown to mitigate chlorpyrifos-induced sensorimotor deficits partly due to its antioxidant and acetylcholinesterase restoration properties.     

The effects of bisphenol A on sex hormone levels of F0 female rats and F1 male rats during weaning period

The effects of bisphenol A (BPA) were examined on sex hormones of F1 generation male rats during weaning period. Female rats were exposed to BPA from day 0 after pregnancy to the weaning period at doses of 50, 100, or 200 mg kg^?1. The sex hormone levels of F1 generation male rats were determined. This study shows that F0 generation female rats fed with 200 mg kg^?1 BPA had a significantly higher serum prolactin (PRL) levels at the end of weaning. Significantly higher levels of serum estradiol (E₂) were also found in female rats fed 100 or 200 mg kg^?1 BPA. Serum levels of E₂ in F1 male generation rats were higher in treatment groups compared to control groups while serum testosterone (T) levels were lower. Follicle stimulating hormone (FSH) in F1 generation rats fed 200 mg kg^?1 was markedly decreased. The relative testicular weights were significantly less in 100 and 200 mg kg^?1 BPA groups. BPA was found to alter the sex hormone levels in F1 male rats during weaning period and thus disrupted endocrine functions.     

Effects of Matricaria chamomilla L. on lipid peroxidation,antioxidant enzyme systems,and key liver enzymes in CCl4-treated rats

In this study, we investigated the effects of Matricaria chamomilla L. extract (MCE) on lipid peroxidation, antioxidant enzyme systems, and several liver enzymes in carbon tetrachloride (CCl₄)-treated rats. Rats were divided into five groups. The first group (control group) was fed on standard feed. The rats in the other groups (CCl₄, MCE50, MCE100, and MCE200) were injected intraperitoneally with 0.8?mL?kg^?1 CCl₄. Moreover, rats in the MCE50, MCE100, and MCE200 groups were gavaged with 50?mg?kg^?1, 100?mg?kg^?1, and 200?mg?kg^?1 MCE, respectively. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, whole blood malondialdehyde (MDA) and glutathione (GSH) levels, and erythrocyte superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activity levels were measured after 14 days of exposure. ALT and AST in the CCl₄ group increased significantly in comparison to the control group (p?4, MCE50, MCE100, and MCE200 groups at different significance levels. In conclusion, the findings suggest that, depending on the dose administered, MCE decreases CCl₄-induced damage and consequent oxidative stress in rats; it affects the antioxidant system positively.     

Persistence of chlorpyriphos in okra (Abelmoschus Esculentus) fruits and soil

Persistence of cypermethrin and chlorpyriphos in okra and soil were studied following the application of pre-mix formulation of insecticides Action 505EC (chlorpyriphos 50%?+?cypermethrin 5%) at single (275?g a.i.?ha^?1) and double dose (550?g a.i.?ha^?1). The average initial deposits of chlorpyriphos in okra were observed to be 0.07 and 0.15?mg?kg^?1 in single and double dose, respectively, which dissipated to 92% after 10 days for both the dosages. Residues of soil under okra crop were found to be 0.15?mg?kg^?1 at the single and 0.36?mg?kg^?1 at the double doses. These residues persisted up to 3 days at single and 5 days at double dose. The half-life (t _1/2) periods of chlorpyriphos on okra and soil were observed to be 0.6 days and 1.9 days for single and double dose, respectively. Residues of chlorpyriphos reached below detectable level (BDL) of 0.01?mg?kg^?1 in okra fruits after 7 days at single dose and in 15 days in double dose. In soil, residues of chlopyriphos persisted up to 5 and 7 days in single and double dose, respectively. Following foliar applications of a insecticide formulation (Action 505EC, (chlorpyriphos 50%?+?cypermethrin 5%) on okra at @ 275 and 550?g active ingredient (a.i.)?ha^?1 resulting in active applications of chlorpyriphos at the rate of 250 and 500?g a.i.?ha^?1 the average initial deposits of chlorpyriphos in okra were observed to be 0.07 and 0.15?mg?kg^?1, respectively. These residue levels dissipated to 92% after 10 days at both the dosages. Residues of soil under the okra crop were found to be 15?mg?kg^?1 at the single and 36?mg?kg^?1 at the double dose. The residues persisted up to 3 days at the single and 5 days at the double dose. The half-life (t _1/2) periods of chlorpyriphos on okra were observed to be 0.6 days for application rates, and 1.9 days for soil. Okra fruits and soil samples collected on the 7th and 15th day after application did not show any chlorpyriphos residues above their determination limits of 0.01 and 0.005?mg?kg^?1, respectively.     

Bromobenzene-induced hepatotoxicity in male rats: the protective effect of flaxseed

The metabolites of bromobenzene (BB) are hepatotoxic. The aim of this study was to determine the efficacy of different doses of flaxseed extract in alleviating BB-hepatotoxicity in male albino rats. Oxidative stress parameters, drug metabolizing enzymes, a pro-inflammatory marker, an apoptotic marker, and DNA fragmentation pattern were also assessed. Animals were divided into five groups treated by intragastric intubation as follows: control, BB-treated 460?mg?kg^?1?BW alone; three animal groups (III, IV, V) were treated concurrently with 460?mg?kg^?1 BB daily for 3 weeks and different doses of flaxseeds extract: 100, 200, or 300?mg?kg^?1?BW. Oral treatment of BB produced a significant decrease in activities of antioxidant enzymes superoxide dismutase and glutathione peroxidase and glutathione levels, while activities of glutathione reductase and drug-metabolizing enzymes; glutathione-S-transferases and cytochrome P450 were enhanced. BB-treatment resulted in enhanced production of nitric oxide and activation of COX-2 and caspase-3. Pre-treatment with different doses of flaxseeds extract prior and during BB-treatment protected liver against BB-induced hepatotoxicity. The lower dose of flaxseed extract (100?mg?kg^?1) was most effective one.     

Acute toxicity and histopathology study of a galactose-specific lectin from the seeds of Tetracarpidium conophorum (African walnut) (Hutch and Dalz)

A lactose-binding lectin (TCL) was purified from the seeds of African walnut, Tetracarpidium conophorum, and acute toxicity studies of the lectin were carried out with Swiss albino male mice. Animals were administered doses of TCL from 500 to 2500?mg?kg^?1 body weight (b.wt.) orally while intraperitoneally the dose ranged from 10 to 600?mg?kg^?1 b.wt. Animals were then assessed for organ and body weight changes, mortality, and histopathology. TCL did not cause any observable toxicity via the oral route; however, when administered intraperitoneally, TCL elicited toxicity with an LD₅₀ of 50?mg?kg^?1 b.wt. Death from intoxication was preceded by convulsion, hypoactivity, salivation, ataxia, and weakness. The animals given lethal doses of the lectin showed profound respiratory depression which was judged to be the primary cause of death. Histopathological analysis indicated that the lungs, liver, and spleen were adversely affected while the kidney and other organs were essentially normal. In all the affected organs, the severity of toxicity was dose-dependent as the effect of the lectin became more pronounced with increase of the dose administered.     

Comparative effects of five chelating agents on testicular toxicity in mice induced by acute exposure to cadmium

The aim of this study was to develop new antidotes for cadmium (Cd) since this metal is known to produce mammalian toxicity. N-p-hydroxymethylbenzyl-D-glucamine dithiocarbamate (HBGD), N-benzyl-D-glucamine dithiocarbamate (BGD), diethyldithiocarbamate (DDTC), 2,3-dimercaptopropanol (BAL), and ethylenediamine-tetraacetic acid (EDTA) were studied for their ability to inhibit the adverse effects induced by Cd on mouse testes. The parameters examined included concentrations of Cd, calcium (Ca), iron (Fe), and zinc (Zn) in testes, lipid peroxidation (LPO) levels in testes, lactate dehydrogenase (LDH) activity in serum and reproductive ability of male mice. Mice injected intraperitoneally (ip) with CdCl₂ (2.5?mgCd?kg^?1) after 30?min or 24?h, were then injected ip with chelating agents (400?µmol?kg^?1). Cd increased the concentrations of testicular Ca, Cd, Fe, Zn, and LPO levels as well as the activity of LDH in serum. HBGD and BGD effectively prevented the increase in above indices, and improved the reproductive ability weakened by exposure to Cd. The results suggested that HBGD and BGD are more effective detoxificants in the case of testicular toxicity in mice induced by acute exposure to Cd.     

Determination of metals in printed wiring boards of waste mobile phones

Metal contents of waste mobile phones represent a major environmental risk, especially considering the adoption of inappropriate management options in developing countries including open burning and disposal into surface water bodies. In this study the metal contents of mobile phone printed wiring board (PWB) samples were assessed. Sixty-two waste mobile phones of 15 brands were collected, dismantled, and their PWB samples were analyzed for Cu, Pb, Ag and Cd. The metal concentrations in the samples varied widely between and within brands. Among these metals, Cu and Pb were found to be at very high concentrations. The range (mean?±?SD) of Cu and Pb concentrations were 94.1–532?g?kg^?1 (250?±?92.3?g?kg^?1) and 7.0–46.2?g?kg^?1 (20.1?±?8.4?g?kg^?1), respectively. All Cu and Pb concentrations exceeded toxicity threshold limit concentration (TTLC) regulatory limits used in characterizing wastes as hazardous in the state of California, USA. The mean Cu and Pb concentrations exceeded the corresponding TTLC limits by factors of 100 and 20, respectively. The Ag and Cd concentrations were in the range 59.4–759?mg?kg^?1 (mean 227?±?104?mg?kg^?1) and ND – 15.6?mg?kg^?1 (2.1?±?3.3?mg?kg^?1), respectively.     

Ecotoxicity of silver nanoparticles on earthworm Eisenia fetida: responses of the antioxidant system,acid phosphatase and ATPase

Ecotoxicity of nanoparticles has received growing attention in recent years. This study investigated the influence of silver nanoparticles (Ag-NP) on earthworm Eisenia fetida. The experiment was performed with five test groups: control (without Ag-NP), 10?nm Ag-NP groups (20, 100 or 500?mg?kg^?1) and positive control (787?mg?kg^?1 AgNO₃). After 14-day acute exposure, activities of various enzymes, including glutathione S-transferase (GST), glutathione reductase (GR), acid phosphatase (AP), and Na⁺, K⁺-ATPase were determined. Effects of Ag-NP with different sizes (10 and 80?nm) were also tested. Data showed that the activity of GR was significantly lower at 500?mg?kg^?1. The activities of AP and Na⁺, K⁺-ATPase were inhibited following the increase of Ag-NP concentration. When treated with Ag-NP with different sizes, activities of AP and Na⁺, K⁺-ATPase of the 10?nm group were significantly lower than the control group, but those of the 80?nm group were similar to the control group. Data indicate that Ag-NP may be harmful to the earthworm E. fetida at 500?mg?kg^?1, and the toxicity of Ag-NP with 10?nm size is greater than 80?nm. In addition, AP and Na⁺, K⁺-ATPase are sensitive biomakers to the effects of Ag-NP.     

Phytochemical screening and toxicological profile of methanolic extract of Picralima nitida fruit-rind (Apocynaceae)

The methanol (M) extract of the fruit-rinds of Picralima nitida (PN) was analyzed phytochemically and evaluated for its toxicity effect in Wistar rats. The rats were administered graded doses (0.75, 1.5, 3, and 6 g kg^?1 p.o) of the extract daily for 6 weeks and the toxicological effect of these varying levels of extract were examined on the serum, hepatic, and renal concentration of biochemical parameters as well as the histopathology of tissue section of these liver, kidney, and lungs. Clinical signs and hematology were also evaluated. Phytochemical analysis revealed that alkaloids and polyphenols were major compounds. Both biochemical and histopathological data presented demonstrate dose-dependent signs of toxicity. Our results show a significant elevation in serum concentration of aspartate amino-transferase, alanine amino-transferase, glucose, creatinine, total cholesterol, and protein with high-dose of PN treatment tested. PN also caused a significant reduction in hepatic malondialdehyde and a slight increase in glutathione concentration at the lowest dose tested. Renal urea level was reduced significantly in test groups. A significant change was observed in the relative weights of the spleen, heart, and kidneys. The total white blood cell count was reduced, whereas the hematocrit level was increased remarkably in animals that received high doses of the extract. The acute toxicity LD₅₀ was estimated at 14.5 and 12.5 g kg^?1 body weight for male and female, respectively. These results show that prolonged usage of this extract at 1.5–6 g kg^?1 dose could cause liver, kidney, and lung injury, while the effect was mild at small dose levels (0.75 g kg^?1). Thus, the extract should be taken with caution bearing in mind that higher doses could affect the liver, kidneys, and lungs.     

Gender-based comparative toxicity of di-ethyl phthalate in Wistar rats

In recent years, the exposure of humans to phthalate esters through environmental contamination has increased. One among them is di-ethyl phthalate (DEP), which is used as a plastisizer for cellulose ester plastic films and sheets, solid rocket propellants, molded and extruded articles, as a component in insecticide sprays and various other substances, as well as in industrial applications. Release into the environment occurs primarily as a result of production and manufacturing of DEP and during the use and disposal of products containing DEP. Therefore, a study was undertaken to evaluate gender-specific toxicity of DEP in Wistar rats. Rats of both sexes, weighing 125–130?g, were administered 50?ppm (w/v) DEP in water ad libitum for a period of 180 days and were given normal diet. Control animals received normal diet and water ad libitum. During the treatment, rats were weighed every week and water consumption per day was measured. After the completion of treatment, liver weight?:?body weight^?1 ratio, liver weight, body weight^?1, liver and serum enzymes, and other biochemical parameters of liver and serum were assessed. It was observed that there was no significant change in body weight^?1, liver weight, liver weight?: body weight^?1 ratio, and water consumption in both sexes. There were significant increases in liver acid phosphatase (ACP) activity and kidney glutathione levels, and nonsignificant changes in liver alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), succinate dehydrogenase (SDH), and lactate dehydrogenase (LDH) activities in DEP-treated male rats, whereas in DEP-treated female rats the liver showed significant decrease in ALP and SDH and nonsignificant changes in AST, ALT, and LDH activities. Serum ACP and LDH levels in DEP-treated male rats were significantly decreased, and in the case of DEP-treated female rats, only serum LDH levels were significantly decreased. There was no significant change in serum ALP, AST, and SDH levels in DEP-treated male and female rats as compared to control rats. Histology of the livers of both male and female rats showed loss of hepatic architecture, degenerative changes in hepatocytes, and vacuolation in hepatocytes in both the centrilobular and periportal areas. It can be concluded from this study that prolonged exposure to DEP at 50?ppm levels can be harmful to animals and humans. This is evident from the present study as certain significant changes in enzyme activities in the liver, serum, and histological alterations in liver were observed.     

Faecal elimination of cypermethrin by cows after pour-on administration: Determining concentrations and measuring the impact on dung beetles

Cattle treatment with antiparasitic drugs is associated with an important risk exposure for dung beetles. Previous studies demonstrated the impact of some avermectin and pyrethroid compounds on several species such as Onthophagus gazella and Neomyia cornicina. However, little information is available regarding the elimination of these compounds in faeces 8 days after a pour-on administration in dairy cows. The present study, utilising a dairy cow model with cypermethrin treatment, demonstrated that concentrations in dry faeces can reach levels of 5?mg?kg^?1 between the first and fourth day after treatment and were present up to 3 months after a single dose of administration at a concentration around 10?µg?kg^?1. Faecal samples were purified with three successive columns (silica gel, anion exchange phase, and basic alumina) and analysed by GC-MS. The limit of quantification of this method was 0.5?µg?kg^?1. The high sensitivity of the method permitted one to see that the risk exposure of cypermethrin to dung beetles is longer than what was noted in the literature. According to other studies, repeated treatment with such agents may lead to the local extinction of dung beetles. Even if the impact of pyrethroid largely depends on the conditions of the ecosystem where the treated cattle are living, adverse effects of these agents may still occur.     

Abstracts to forthcoming papers

Food is the major source of metal exposure for the nonsmoking general population. Food samples of plant and animal origin from Ismailia, Egypt, were analyzed for the content of cadmium (Cd), lead (Pb), chromium (Cr), zinc (Zn), and copper (Cu) using AAS. The Cr, Zn, and Cu concentrations were in the range of 1.7–249?µg?kg^?1 wet weight (ww), 2–66?mg?kg^?1?ww, and 0.5–3.46?mg?kg^?1?ww, respectively. The mean daily intake of Cr, Zn, and Cu was 28.9?µg day^?1, 8.55?mg day^?1, and 1.7?mg day^?1, respectively. The intake estimates are within the range of the recommended intake established internationally. Concentrations of Cd and Pb were in the range of 10–321?µg?kg^?1?ww and 31–1200?µg?kg^?1?ww, respectively. The weekly dietary intake for Cd and Pb (4.02 and 20.4?µg?kg^?1 b.w, respectively) is lower than the FAO/WHO PTWI. Bread is the foodstuff that provided the highest rate of Pb and Cd (62 and 46% of the daily intake) to adults in Ismailia city.     

Chronic mixture toxicity study of Clophen A60 and diethyl phthalate in male rats

Chemical mixtures are an important area of research as individuals are exposed to low doses of persistent chemical agents known as environmental pollutants throughout their life time. Polychlorinated biphenyls (PCBs) and diethyl phthalate (DEP) are ubiquitous environmental pollutants that could be present in the same environmental compartment; hence organisms may get simultaneously exposed to both. Therefore, a study was undertaken to see whether PCB and DEP together show interactive chronic mixture toxicity in male Wistar rats. Healthy male Wistar rats weighing 70–100?g were randomly assigned to four groups of six each. Control rats were fed on normal diet and water ad libitum. Oil control rats were maintained on a normal diet mixed with corn oil. Rats were given Clophen A60 (PCB) and DEP dissolved individually in corn oil mixed with the diet at 50?mg?kg^?1 of the diet/day, as well as a mixture in corn oil mixed with the diet both at 50?mg?kg^?1 of the diet/day. After 150 days of treatment animals were sacrificed and enzymes and other biochemical parameters in the serum and liver were assessed. Liver weight to body weight ratio showed a significant increase in Clophen A60 and in Clophen A60?+?DEP treated rats. In the DEP, Clophen A60 and Clophen A60?+?DEP treated groups there was significant increase in liver and serum alanine aminotransferase (ALT) and acid phosphatase (ACP) activity. Aspartate aminotransferase (AST) was significantly increased in the liver and serum of DEP treated rats only. Cholesterol levels were significantly increased only in the serum and the liver of DEP treated rats. Triglyceride levels were significantly increased in the serum of treated rats and only in the liver of Clophen A60 and Clophen A60?+?DEP treated rats. Liver glycogen levels were significantly increased in DEP and Clophen A60?+?DEP treated rats. In all treated animals, there was a significant decrease in liver glutathione reductase (GR). Histology of liver showed severe vacuolations, fatty degeneration and loss of hepatic architecture in Clophen A60 and Clophen A60?+?DEP treated rats, whereas in DEP treated rats only loss of hepatic architecture and granular deposits in the hepatocytes was predominant with mild vacuolations of centrilobular and periportal area. It is evident from this study of mixture toxicity of Clophen A60 and DEP that there is no significantly enhanced toxicity due to the interaction of these two compounds. On the other hand, to some extent there is alleviation in toxicity as evidenced by enzyme ACP and AST levels in the liver. The hepatocellular damage and biliary congestion caused by these two compounds, which can be confirmed by significantly increased liver weights and elevated serum and liver enzyme levels as well as histology, was almost the same between individual and mixture treated group.     

Toxicological studies of zinc oxide nanomaterials in rats

In this study, we have evaluated the ability of zinc oxide (ZnO) nanoparticles to induce pulmonary and extrapulmonary toxicities was examined in rats following intratracheal (IT) instillation. Lungs of rats were instilled IT with either phosphate-buffered saline (PBS)?+?1% Tween 80, ZnO nanoparticles, carbonyl iron or quartz particles at a dose of 1 or 5?mg?kg^?1 body weight. Following exposure, bronchoalveolar lavage (BAL) fluid, blood samples and organs including lung, liver, kidneys, heart, pancreas, and brain were collected at 24?h, 1 week, or 1 month of post instillation of nanoparticles and different parameters estimated to assess toxicity. BAL fluid was analyzed for lactate dehydrogenase (LDH) and alkaline phosphatase (ALP) to assess pulmonary toxicity. Exposures to ZnO or quartz particles produced transient dose-dependant increase in BAL fluid LDH and ALP activities at all post exposure periods. Blood samples were analyzed for the tissue damage biomarkers to assess extrapulmonary toxicity. Histopathological examination of lung, liver and kidneys revealed dose-dependent degeneration and necrosis which worsened at 1 week post-instillation periods but recovered at 1 month post instillation. Histopathological examination of rat pancreas, heart, and brain exposed to quartz or ZnO particles showed no marked changes. Data suggest the instillation of ZnO nanoparticles produced a greater pulmonary toxicity in rats comparable with quartz; and extrapulmonary toxicities of these ZnO nanoparticles might be due to translocation into liver and kidney.     

Lead-induced alterations in protein-deficient rat liver–role of zinc

This study was designed to determine the protective effects of zinc (Zn) using liver marker enzymes in the serum and liver along with hepatic elemental profile in lead (Pb)-treated protein-deficient (PD) Sprague–Dawley male rats. Zn in the form of zinc sulfate at a dose of 227?mg?L^?1 in drinking water was administrated to control, PD as well as Pb-treated PD rats for 8 weeks. Pb treatment was given orally as lead acetate at a dose level of 100?mg?kg^?1 body weight to control and PD rats. The effects of different treatments were studied on the activities of enzymes that included alkaline phosphatase (ALP), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in serum. The status of different elements (Cl, K, Mn, Fe, Cu, Zn, Se, Rb, Pb) in liver was also studied. Rats given PD diet and Pb showed significant inhibition in serum ALP activity associated with significant elevation in both AST and ALT activities. Serum ALP activity showed a significant inhibition week 1 until week 8 in Pb-treated PD rats. In contrast, serum AST activity was elevated both at 3 and 8 weeks while serum ALT activity was elevated at 8 weeks in Pb-treated PD rats. Pb treatment to PD rats elevated hepatic ALP, AST and ALT activities but depressed hepatic AST. Zn supplementation to Pb-treated PD rats restored the altered enzyme activities. The levels of K, Fe, Cu, Zn, Se and Rb were altered in protein deficiency. Furthermore, treatment with Pb to these animals depressed the Cu levels. Zn treatment to Pb-treated PD animals tended to restore the levels of altered elements. Hence, the present study clearly suggests that Zn plays an important role in regulating the liver marker enzymes and essential elements under conditions of Pb toxicity and protein deficiency.     

Biochemical alterations in rat brain following aluminum exposure: Protection with centrophenoxine

Aluminum (Al) is a neurotoxicant potentially affecting ionic, cholinergic, and dopaminergic neurotransmission in the central nervous system. These alterations are known to be associated with learning ability, adaptive responses, and other aspects of behavior. The present experiment was designed to study the neurotoxic consequences of Al exposure on neurotransmitters like dopamine (DA), serotonin (5-HT), norepinephrine (NE) along with the activity of acetylcholinesterase (AChE). Furthermore, Centrophenoxine (CpH) was administered as a post treatment to evaluate its potential in Al-induced neurotoxicity. The cognitive functions and memory loss were also studied after both Al and CpH administration. Al was administered orally at a dose of 40?mg?kg^?1?day^?1 for a period of 8 weeks, whereas CpH was administered intraperitoneally at a dose of 100^?1?mg?kg^?1?day^?1 for a period of 6 weeks. The study was carried out in four regions of the brain, namely cerebrum, cerebellum, medulla oblongata, and hypothalamus. A significant reduction in AChE activity and different neurotransmitters was observed after Al exposure in the regions. CpH as a post treatment proved beneficial in restoring these alterations. Al exposure also affected the cognitive functions and short-term memory, which were significantly improved following CpH post treatment.