Combined effects of 2,3,7,8-tetrachlorodibenzo- p -dioxin and polychlorinated biphenyl congeners in rats

The objective of this work was to evaluate potential interactions between 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and polychlorinated biphenyls congeners (PCBs) in rats. Groups of five adult female rats were given 0, 2.5, 25, 250, or 1000?ng TCDD/kg body weight/day or TCDD in combination with a mixture of PCB congeners at a concentration of 2 or 20?µg?kg^?1 body weight/day by gavage for 28 days. After the 28-day treatment period, the rats were killed for the analysis of biochemical, liver enzyme activities, and hematological and pathological end points. Growth suppression, increased absolute and relative liver weights, and decreased thymic weight were observed in the 1000?ng TCDD group alone, or the groups receiving a mixture of 1000?ng TCDD and 2 and 20?µg PCBs. TCDD-increased liver and thymic weights were not altered by PCBs; however, growth suppression was more pronounced in animals receiving 1000?ng TCDD and 2?µg PCBs. Increased hepatic microsomal methoxy resorufin-O-demethylase and ethoxy resorufin-O-deethylase activities occurred in 250 and 1000?ng?kg^?1 TCDD-treated animals, which were antagonized by PCBs. Effects of 250?ng TCDD on serum cholesterol and liver uridine diphosphate glucuronosyl transferase activity were reduced by 20?µg PCBs. Treatment with 1000?ng TCDD increased serum albumin, decreased liver vitamin A, increased kidney vitamin A, and liver microsomal glutathione-S-transferase activity, which were not affected by PCBs. Decreased hemoglobin, platelet, packet cell volume, and red cell indices were observed in TCDD-treated rats, but no interactive effects were seen. Histopathological evaluation revealed that liver, thyroid, and thymus were the target organs, but the effects of co-exposure to PCBs and TCDD were variable. These results indicate that the mixture effects of PCBs and TCDD may be additive, synergistic, or antagonistic depending on the dose level and end points measured.     

伊维菌素对雄性吉富罗非鱼生理生化指标的影响

为探讨抗寄生虫药物伊维菌素(IVM)对鱼类的毒性效应,以雄性吉富罗非鱼(Oreochromis niloticus)为实验对象,设定了A(空白对照)、B(乙醇对照)、C(0.1 mg·kg~(-1))、D(0.5 mg·kg~(-1))、E(1 mg·kg~(-1))5个实验组,研究IVM对吉富罗非鱼肝脏和血液生理生化的影响。研究发现:正常生理状态下吉富罗非鱼肝脏中的丙二醛(MDA)含量较低,IVM作用后除最高剂量E组中MDA含量在4 h、16 h和24 h时极显著高于对照组外,其余各组均未受到显著影响。较低注射剂量C组中超氧化物歧化酶(SOD)活性均得到了诱导,且均显著高于对照组,较高注射剂量组中除E组在第4 h、16 h和24 h SOD活性显著高于对照组外,其余均未发现有显著变化。肝脏中谷草转氨酶(AST)和谷丙转氨酶(ALT)在IVM作用下均发生了一定的变化,尤其是E组均显著低于对照组。与肝脏中的相反,血液中的AST则随剂量的升高而呈现增加的趋势,在某些时间点与对照组相比显著升高,而血液中ALT除C、D组个别时间点外其余的均未有显著变化。B、C、D、E 4组肝脏中的碱性磷酸酶(ALP)相对A组均发生了显著下降,但C、D、E组与B组除个别时间点外均未有显著差异,因此肝脏中的ALP变化可能是无水乙醇作用的结果,而非IVM。血液中ALP则均未有显著变化。研究表明高剂量的IVM对吉富罗非鱼的肝脏造成了一定影响,因此在实际使用过程中应选择合适的给药方式以及合理的给药剂量。     

Protective effects of curcumin on antioxidant status,body weight gain,and reproductive parameters in male rats exposed to subchronic 2,3,7,8-tetrachlorodibenzo-p-dioxin

The aim of this study was to investigate the effects of curcumin (CUR) on antioxidant status, body weight (BW) gains, and some reproductive parameters in male rats exposed to subchronic doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Thirty-two rats were divided into four groups. The first group was kept as control. The second group (TCDD group) was given TCDD at a dose of 50 ng·kg^?1 BW per day; the third group (CUR group) was treated with CUR at a dose of 80 mg·kg^?1 BW per day. The fourth group (TCDD + CUR group) was given TCDD and CUR at the same doses simultaneously. Malondialdehyde (MDA) levels were significantly increased in the TCDD group. In addition, TCDD exposure decreased liver superoxide dismutase (SOD) activity, catalase (CAT) activities of kidney and brain, glutathione peroxidase (GSH-Px) activities of liver, kidney, and brain, and glutathione levels of liver, kidney, and heart. However, CUR treatment with TCDD exposure decreased MDA levels in all tissues and increased SOD activities of liver, kidney, and brain, CAT activity of heart, and GSH-Px activities of heart and brain. TCDD caused a decrease in BW gain, and CUR partially eliminated this effect of TCDD. In addition, while reproductive organ weights, sperm concentration, and sperm motility tended to decrease with TCDD exposure, these effects tended to be close to normal levels by CUR treatment. In conclusion, CUR was seen to be effective in the treatment and prevention of toxicity induced by subchronic TCDD exposure.     

Effects of deltamethrin on serum calcium and corpuscles of Stannius of freshwater catfish,Heteropneustes fossilis

Adult male deer mice were exposed every other day for a period of 11 days to either 7,12-dimethylbenzanthracene (DMBA; CAS# 57-97-6) or benzo[b]fluoranthene (BbF; CAS# 205-99-2) (0, 0.3, 1, 3, 10, or 30?mg?kg^?1). Immune endpoints assessed were lymphocyte proliferation, macrophage pinocytosis, and the antibody plaque-forming cell (PFC) response. Cytochrome P450 (CYP450) activity was assessed using ethoxyresorufin-O-deethylase (EROD) and pentoxyresorufin-O-deethylase (PROD). Macrophage pinocytosis was not altered by either compound. Both T- and B-cell proliferations were significantly increased by DMBA at 0.3 or 1?mg?kg^?1 and by BbF at 10 or 30?mg?kg^?1, but decreased by DMBA at 30?mg?kg^?1. Sheep red blood cell (SRBC)-specific-IgM production, as measured by the PFC response, was the most striking adverse immune effect observed and was significantly suppressed compared to control at all treatment concentrations for both compounds. EROD activity was markedly induced by DMBA at 30?mg?kg^?1, while BbF produced induction at 1, 10, or 30?mg?kg^?1. No marked effect on PROD activity was noted following DMBA treatment, but BbF-induced PROD activity at 1, 10, or 30?mg?kg^?1. Unexpectedly, four of six mice in the 30?mg DMBA?kg^?1 group did not survive to the end of the experiment, and one animal died in both the 3 and 10?mg?kg^?1 treatments. The calculated LD₅₀ was 20.8?mg DMBA?kg^?1. The PFC response in deer mice was a more sensitive endpoint than CYP450 activity, suggesting that utilization of CYP450 endpoints in risk assessment without assessment of immune function, specifically antibody production, might possibly underestimate the risk to wild rodents environmentally exposed to polycyclic aromatic hydrocarbons.     

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.     

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.     

Therapeutic effect of melatonin against aluminum-induced neurotoxicity in cerebellum of albino mice

The therapeutic effect of melatonin (MEL) against aluminum (Al)-induced neurotoxicity was investigated in mouse cerebellum. Two groups of male albino mice were intraperitoneally injected with Al acetate or MEL alone, at doses of 3.5 or 7?mg?kg^?1?day^?1, respectively, for 6 weeks. During this period, another group of animals received a combination of both Al and MEL (3.5?+?7?mg?kg^?1?day^?1). At the end of the treatment cerebellum was removed and processed to examine the oxidative stress markers: superoxide dismutase (SOD), catalase (CAT), and thiobarbituric acid-reactive substances (TBA-RS). Oxidative stress increased significantly with administration of Al which was estimated by increased TBA-RS and reduction in the activities of SOD and CAT. However, these alterations were significantly reversed significantly following MEL treatment which was observed in co-administered group. Protective effects of MEL were also observed at electron microscopic level. Ultrastructural studies revealed an increase in vacuolization, chromatin condensation within the nucleus, degenerated purkinje cell, degenerated axon and degenerated granule cells in the cerebellum of Al-treated mice group whereas concurrent administration of MEL with Al reduced these changes. The results of the present investigation emphasize the potential use of MEL as a supplement in therapy of free radical based neurological disorders in which oxidative stress is involved.     

内质网应激在PFOS致大鼠肝损伤中的作用

通过全氟辛烷磺酸(PFOS)28 d大鼠经口染毒评价PFOS肝损伤效应,探讨内质网应激在PFOS毒效应中的作用。Wistar大鼠随机分组,分别以0 mg·kg~(-1)、5 mg·kg~(-1)和10 mg·kg~(-1)PFOS灌胃染毒28 d。HE染色观察大鼠肝脏形态改变。ELISA法测定各组丙氨酸转氨酶(ALT)、天门冬氨酸转氨酶(AST)、碱性磷酸酶(ALP)和淀粉酶(AMY)含量变化。紫外分光光度法测定肝组织匀浆中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性变化。RT-PCR检测肝脏内质网应激标志蛋白表达水平。结果表明,PFOS造成大鼠体重降低、肝重增高(P0.05),组织切片显示肝细胞出现脂质沉积。PFOS不同剂量组大鼠ALT随暴露浓度增加,分别为(50.96±10.02)U·L~(-1)、(71.73±11.55)U·L~(-1),显著高于对照组(P0.05),AST、ALP含量与对照组相比显著上升(P0.05),高剂量组AMY水平为(833.46±63.05)U·L~(-1),与对照组相比显著降低(P0.05)。GSH-Px和SOD水平随PFOS浓度增加出现了显著降低(P0.05),而MDA水平显著升高(P0.05)。内质网应激标志蛋白表达均较对照组显著上升(P0.05)。以上结果说明PFOS可导致大鼠肝细胞损伤,其机制可能与内质网应激调控有关。     

Inhibition of cyclooxygenase-2 protects against cocaine hepatotoxicity in CF-1 mice

Gender differences in oral cocaine hepatotoxicity have been observed and lipopolysaccharide (LPS) was shown to potentiate cocaine hepatotoxicity in male CF-1 mice. Since cocaine and LPS inflict hepatocellular damage through the production of harmful reactive species, the role of cyclooxygenase-2 (COX-2) in gender-dependent cocaine hepatotoxicity was investigated. COX-2 increases nitric oxide (NO) synthesis and pro-inflammatory mediator production in response to hepatocellular insult. Male and female CF-1 mice were orally administered 20 mg kg^?1 cocaine hydrochloride once daily for 7 days. Four hours after the last cocaine administration, the mice received 12 × 10⁶ EU LPS intraperitoneally (cocaine + LPS). Mice receiving meloxicam (7.5 mg kg^?1, p.o.), a selective COX-2 inhibitor, were pretreated 1 h before each cocaine administration. Meloxicam prevented liver damage in males produced by cocaine and cocaine + LPS as evidenced by microscopic appearance and biochemical indices equivalent to saline treatment. Acetaminophen (APAP) was administered orally as a positive control which shows no gender dependency and elicited a hepatotoxic response in both males and females. Altered biochemical indices suggest that COX-2 is activated, possibly to a greater extent in females versus males in APAP-induced hepatotoxicity. Meloxicam prevented all oxidative stress changes induced in males following APAP. The results suggest that the induction of COX-2 is responsible, in part, for cocaine hepatotoxicity with and without LPS exposure in male mice.     

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.     

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.     

Toxicokinetics,metabolism, and microsomal studies of chlorpropham in rats

A study on the toxicokinetic behavior, metabolism of chlorpropham, and its effect on cytochrome P₄₅₀ from liver microsomes was carried out in albino rats after a single and consecutive oral administration at 500?mg?kg^?1 body weight for 10 and 20 days. Chlorpropham was detected in the blood at 0.08?h (11.43?±?1.72?µg?mL^?1) reaching a maximum concentration at 2?h (30.90?±?2.55?µg?mL^?1) and a minimum at 48?h (1.95?±?0.20?µg?mL^?1) after a single oral administration of 500?mg?kg^?1. The absorption rate constant (K _a) was 0.66?±?0.48?h^?1. The Vd _area (18.01?±?2.78?L?kg^?1) and t _1/2 β (12.23?±?1.96?h) values suggested a wide distribution and long persistence of the compound in the body, respectively. The higher Cl_R (0.82?±?0.00?L?kg^?1?h^?1) compared to Cl_H (0.18?±?0.02?L?kg^?1?h^?1) value indicated that a major portion of chlorpropham was excreted through the urine (30%) compared to the faeces (2.81%). Chlorpropham residue was detected in all tissues of rat at 0.25?h while its metabolite, meta-chloroaniline was detected in liver, kidney, heart, lung, and spleen tissue at 0.25?h. Meta-chloroaniline was not detected in skeletal muscle, brain, fat, and stomach tissue at any time of the observation period. Maximum concentrations of chlorpropham and meta-chloroaniline were detected at 2?h (except in the spleen), and minimum concentrations of chlorpropham at 24 (heart, lung, spleen, skeletal muscle, and stomach) and 48?h (liver, kidney, brain, and fat tissue) respectively; and meta-chloroaniline at 24?h (except heart and spleen). The tissue half-life of chlorpropham in rat varied from 3.80 to 11.60?h. Repeated oral administration of chlorpropham at 500?mg?kg^?1 for 10 and 20 days caused an induction of the liver microsomal pellet of rat.     

Effects of nanopesticide chlorfenapyr on mice

The effects of chlorfenapyr nano preparation on mice were examined. The animals were administered with different doses of 4.84, 9.68, or 19.36?mg?kg^?1 of chlorfenapyr common preparation or nano preparation intraperitoneally (IP). Micronucleus (MN) test and comet assay (CA) experiments revealed that at the same dose, similar DNA damage in the peripheral blood lymphocytes of the mouse and chromosome damage in bone marrow cells of the mouse occurred with chlorfenapyr nano preparation; however, the severity of these effects was less than that found in common preparation. It is noteworthy that there were no differences in apoptotic ratio and live cell percentage in the liver cells of the mouse between these two pesticide formulations using flow cytometry. Data indicate that chlorfenapyr nanoformulation is less toxic to mouse cells than the common formulation.     

Effects of dietary copper exposure on accumulation,growth, and hematological parameters in Cyprinus carpio

The influence of dietary copper (Cu) exposure on accumulation, growth, and hematological parameters was investigated in Cyprinus carpio after sub-chronic ingestion of 0, 250, 500, 750 or 1000?mg?kg^?1 for 60 days. The profile of Cu accumulation among tissues in C. carpio was dependent on the exposure period and Cu concentration. Liver of C. carpio was the predominant storage tissue and the order of Cu accumulation in tissues was liver?>?intestine?> gill?>?kidney?>?muscle. Cu concentration at >125?mg?kg^?1 reduced growth rate, and was inversely related to growth. The RNA?:?DNA ratios were not affected by exposure and there was no correlation between growth rate and RNA?:?DNA ratio in liver and muscle. There were no significant effects of exposure on blood parameters except for magnesium. Cu exposure time and dose increased the serum glutamic-oxaloacetic transaminase (SGOT) and serum glutamic-pyruvic transaminase (SGPT) activity levels.     

Chlorpyrifos induces oxidative stress in rats

This study was carried out in male Wistar rats to determine the potential effects of chlorpyrifos (CHP) on oxidative stress, as was reported for organophosphorus (OP) pesticides. Following an acute, daily 3- or 14-day exposure with CHP at doses of 2.5, 5, or 25 mg kg^?1 data showed significant increases in malondialdehyde levels at both exposure durations and at all doses, except for 2.5 mg kg^?1, in hepatic and aorta, kidney, and plasma samples. The nitrites (NO) showed elevation at 25 mg kg^?1 in aorta, at 3- and 14-day exposure, in hepatic tissue with all doses at 3-day exposure, but not at 14-day with a 5 mg kg^?1 dose. In plasma, increases occurred only at 25 mg kg^?1 at both exposure times, and in kidney at all doses and both exposure durations. Superoxide dismutase (SOD) enzyme activity in the aorta sample was statistically significant at all doses at 3 days and at 14 days, except at 2.5 mg kg^?1; and in hepatic tissue only at 25 mg kg^?1 dose at both durations. In plasma SOD activity was elevated at all doses at 3 days, but at 14 days only at 25 mg kg^?1. Data suggests that oxidative stress may be involved in the effects of CHP on rats.     

Speciation of mercury in South African coals

Total mercury (Hg_TOT) concentrations were determined by inductively coupled plasma mass spectrometry (ICP MS) for South African Highveld coals. The distribution of Hg in coals was investigated using a four-stage sequential leaching protocol and isotope dilution/gas chromatography coupled to ICP MS (ID-GC-ICP MS). The results show that Hg_TOT ranged from 144 to 303?µg?kg^?1 with a mean of 199?±?26?µg?kg^?1, while Hg_TOT leached from coals using different solvents ranged between 103 and 310?µg?kg^?1 (mean: 218?±?60?µg?kg^?1). Hg leaching rates of 53–78% were achieved in crushed coals. Hg⁰, Hg²⁺, and CH₃Hg⁺ were identified in all coals. CH₃Hg⁺ in studied coals ranged between 0.1 and 0.4 (mean: 0.2) µg?kg^?1. GC ICP MS chromatograms also showed unknown Hg peaks which were identified as other organomercury species such as ethylmercury. Modes of occurrence of Hg in coals were variable with the organic-bound (37–40%) and the sulfide-bound (37–39%) being the dominant mercury forms. Increasing the HCl concentration in the used protocol increased the amount of Hg leached (16%) during this step.     

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.     

Antioxidant rich diet supplements (Spirulina and tamarind fruit pulp) mitigate hematological disorders in fluoride exposed mice

The effect of antioxidant rich diet supplements of Spirulina and tamarind fruit pulp at 230 mg kg^?1 body weight, separately as well as in combination, on various hematological parameters of Swiss albino mice exposed to fluoride for seven days at daily doses of 190 mg kg^?1 body weight and for 90 days at daily doses of 94 mg kg^?1 body weight is reported. Compared with controls, fluoride exposure decreased erythrocyte (12%–18%), leukocyte (16%) and platelet counts (7%, only for short-term exposure), hemoglobin (2%–17%) and packed cell volume (2%–14%) in Swiss albino mice reared on standard feed but these were altered little in the diet supplement groups. Fluoride exposure decreased lymphocytes in both standard feed (16%–21%) and diet supplement groups (5%–19%, but only after long-term exposure). Fluoride withdrawal led to recovery of the post-treated mice from long-term exposure. Spirulina alone and also in combination with tamarind fruit pulp was found more effective than tamarind alone in reducing hematological disorders in fluoride treated mice.     

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.     

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.