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.     

Potential hepatoprotective effects of vitamin E and Nigella sativa oil on hepatotoxicity induced by chronic exposure to malathion in human and male albino rats

Malathion is an organophosphorus (OP) insecticide and has a wide range of use in agriculture, veterinary medicine, and public health. Malathion and other OP insecticides produce hepatotoxic effects. The objective of the present study was to investigate the protective effects of Nigella sativa oil and α-tocopherol (vitamin E) on the hepatotoxicity induced by malathion on workers involved in the formulation of pesticides, chronically exposed to malathion, and in male albino rats orally administrated malathion. This study was conducted on both human and experimental animals, the human study was conducted on 30 control subjects working as administrators and 45 subjects working in formulation of pesticides and exposed to malathion (≥3 years), all were males with age ranges from 30 to 60 years. The 45 males working in pesticides formulation were classified into three groups; (1) 15 workers exposed to pesticides (2) 15 workers exposed to pesticides and received vitamin (E), in a dose of 10 mg kg?1 day^?1 orally for 60 days, and (3) 15 workers exposed to pesticides and received 100 mg kg^?1 day^?1 of N. sativa oil for 60 days. The animal experiment was conducted on 40 adult male albino rats weighing 150–200 g. They were divided into four groups (10 rats in each group). First group served as the control group, the second group received malathion in a dose of 50 mg kg^?1 orally per day for 60 days, the third group received malathion (in the same dose and route of administration) and vitamin E in a dose of 10 mg kg^?1 day^?1 orally for 60 days, and the fourth group received malathion (in the same dose and route of administration) and N. sativa oil in a dose of 100 mg kg^?1 day^?1 orally for 60 days. Liver function tests (alanine aminotransferase [ALT], aspartate aminotransferase [AST], serum alkaline phosphatase [ALP], albumin, globulin, albumin/globulin ratio, and total proteins), antioxidant enzymes (catalase (CAT), superoxide dismutase (SOD), and total glutathione peroxidase (GPx)), and lipid peroxidation [MDA] were analyzed in both human and animal experiments. The results of both human and animal study revealed that, exposure to malathion produced significant increases in AST, ALT, and lipid peroxidation. There were significant decrease in albumin, albumin/globulin ratio, total protein, and antioxidant enzymes. There was no significant change in ALP. In addition exposed workers showed significant decreases in serum globulin. Nigella sativa oil or vitamin E administration showed significant improvement of liver function tests, lipid peroxidation, and antioxidant enzymes impairment induced by malathion. Thus, dietary supplement, N. sativa oil, or vitamin E may represent a potential therapeutic agent in reducing malathion-induced hepatotoxicity.     

The effect of chronic formaldehyde exposure on the hippocampus in chronic cerebral hypoperfusion rat model

The aim of this study was to evaluate the effect of chronic formaldehyde (FA) exposure on the hippocampus in the chronic cerebral hypoperfusion rat model. Seventy-two male Sprague-Dawley rats were randomly divided into four groups: (A) sham-operated bilateral common carotid artery occlusion (BCCAO) with room air inhalation, (B) BCCAO with room air inhalation, (C) sham-operated BCCAO with FA inhalation at a concentration of 10?mL?vapor?m^?3, 1?h per day for 90 days, and (D) BCCAO with FA inhalation. Decreased mobility, injected conjunctivae, and overreaction were observed in groups C and D rats after 30 days of FA exposure. The level of malondialdehyde (MDA) increased significantly in group D at 90 days after FA exposure. The expression of Bax protein increased, while Bcl-2 and NR2B proteins decreased significantly in group D compared to group B or C. Neuronal nuclear antigen (NeuN) positive cells decreased significantly in group D. Neuronal loss, oxidative stress, and the expression of proteins were more prominent at 90 days after FA exposure, especially in group D. Oxidative stress-induced neuronal damages in the hippocampus may be a possible mechanism of neurotoxicity as a result of chronic FA exposure. Chronic exposure of FA caused more neuronal damage in the chronic cerebral hypoperfusion rat model.     

羰基镍急性中毒对大鼠骨髓细胞的DNA损伤

通过动物实验观察不同剂量羰基镍对大鼠骨髓细胞DNA损伤程度。采用SD大鼠,以135 mg·m~(-3)和250 mg·m~(-3)羰基镍为染毒组,250 mg·m~(-3)氯气为阳性对照组,静态方式染毒30 min。未染毒组为正常对照组,大鼠染毒后1、2、3和7 d分别采集样本。采用单细胞凝胶电泳检测每组大鼠骨髓细胞DNA的损伤程度。彗星尾长和Olive尾矩2个指标的分析结果表明,大鼠骨髓细胞DNA损伤程度随着羰基镍染毒剂量的增加而增加,在4个时间点各剂量组间均有显著差异(P0.05)且随时间的变化有一定的规律,损伤程度在3 d时达到最大,而后缓慢下降。羰基镍急性中毒对大鼠骨髓细胞DNA有一定的损伤,且存在剂量-效应关系,各剂量组损伤程度有一定的时间效应规律。     

Induction of oxidative stress by benzo(a)pyrene in the epididymis of Wistar rats

The present study was undertaken to evaluate the effect of sub-chronic exposure to benzo(a)pyrene on the antioxidant system and histology of rat epididymal sperm. Intraperitoneal administration of benzo(a)pyrene to male Wistar rats at doses between 1 and 100 µg/kg body weight for 60 days entailed a decrease in the weight of the epididymis (caput and cauda), seminal vesicle, and prostate, while the body weight was not affected. Epididymal sperm reserves were reduced in a dose-dependent manner. Indicators of lipid peroxidation were increased while activities of superoxide dismutase and catalase in all three epididymal regions decreased. Histological malformations were observed in the epididymis. Exposure to benzo(a)pyrene deranges the antioxidant defense system and induces histological changes in the epididymis.     

Subacute chlorpyrifos-induced alterations in serum lipids and some oxidative stress biomarkers in male Wistar rats: beneficial effect of acetyl-L-carnitine

The present study evaluated the beneficial effect of acetyl-L-carnitine (ALC) on subacute chlorpyrifos (CPF)-induced alterations in serum lipid profiles and some biomarkers of oxidative stress in Wistar rats. Twenty-eight adult male rats divided into four groups of seven animals each (group I–IV) were used: I (S/oil) received soya oil (2 ml kg^?1), II (ALC) received ALC (300 mg kg^?1); III (CPF) received CPF (8.5 mg kg^?1 ～ 1/10th LD₅₀); IV (ALC+CPF) was pretreated with ALC (300 mg kg^?1) and then exposed to CPF (8.5 mg kg^?1), 30 min later. The treatment was orally for 28 days duration. Sera obtained from blood samples were evaluated for the levels of triglyceride (TG), total cholesterol (TC), high density lipoprotein-cholesterol (HDL-c), malondialdehyde (MDA), and the activities of superoxide dismutase (SOD) and catalase (CAT). The levels of low density lipoprotein-cholesterol (LDL-c), very low density lipoprotein-cholesterol (VLDL-c), and atherogenic index (AI) were calculated. The result showed that elevated levels of TG, TC, LDL-c, VLDL-c, AI, and MDA, and the decreased levels of HDL-c, CAT, and SOD induced by CPF were modulated by ALC. It was concluded that ALC ameliorated the alterations in serum lipid and oxidative stress induced by CPF exposure in the rats, partly through its antioxidant properties.     

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.     

PM_(2.5)和甲醛联合暴露致小鼠肺损伤及其分子机制的研究

我国城市当前普遍存在室外大气PM_(2.5)与室内甲醛(FA)联合污染状况,二者均被报道在单独暴露下可以导致肺损伤并诱导和诱发哮喘的急性发作,但其联合污染的具体效应,以及分子机制目前尚不清楚。为探究PM_(2.5)和/或甲醛暴露对小鼠的肺损伤及其可能的机制,分别将雄性Balb/c小鼠分为以下6组:对照组,AZD8055组,PM_(2.5)组,FA组,PM_(2.5)+FA组,PM_(2.5)+FA+AZD8055组。染毒结束后,观察肺组织病理学变化;检测肺组织氧化损伤,活性氧(reactive oxygen species,ROS),还原型谷胱甘肽(glutathione,GSH)和丙二醛(malondialdehyde,MDA)的含量,DNA损伤,DNA-蛋白质交联(DNA-protein crosslink,DPC)系数和8羟基脱氧鸟苷(8-OH-d G)的含量,以及细胞凋亡、半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)的含量。结果表明,当吸入气态甲醛浓度为3 mg·m-3,气道滴注PM_(2.5)浓度为2.5 mg·m L-1时,肺组织出现不同程度的支气管重塑和炎症细胞浸润。ROS显著上升,GSH显著下降,DPC、8-OH-d G以及Caspase-3都显著上升。添加AZD8055后,肺组织损伤效应更加显著。PM_(2.5)复合甲醛的暴露导致小鼠肺损伤具有协同作用,氧化应激及其下游的DNA损伤可能是甲醛联合PM_(2.5)致小鼠肺损伤的一种重要机制。     

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.     

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.     

Hematoxicity and hepatoxicity attributed to zinc and cadmium in the Norwegian rat

This study was carried out to determine changes in the blood and liver of rats given oral doses of cadmium (Cd) and zinc (Zn). Thirty 3 month old rats were kept six to a compartment in a well-demarcated five compartment cage labeled A, B, C, D, and E. After 2 weeks of acclimatization, and with ad libitum administration of water and feed, group A and B rats were, respectively, exposed to 100 mg CdSO₄ and 2200 mg ZnSO₄, respectively, mixed with their feed. Group C rats were fed with a combination of 100 mg CdSO₄ and 2200 mg ZnSO₄ mixed with their feed, while group D rats were exposed to 100 mg CdSO₄ mixed with their feed for 48 h, and after they were given 2200 mg ZnSO₄ for 96 h. Group E rats served as control and were fed a normal diet. Analysis of blood samples after 5 days showed that in rats of groups A, B, C, and D, WBC count increased from 6800 to 12,400 mm^?3 and platelets from 26,000 to 88,000 mm^?3. Reduction in blood counts were found for RBC from 13.8 to 4.7 × 10⁶ mm^?3, hemoglobin from 15.6 to 11.4 dL^?1, and PCV from 47 to 34%. ESR was the same 1.0 mm h^?1 in all groups. Severe damage to the liver was also shown by severe degeneration of hepatocytes and increase in Kuppfer cells. The above observations were mildest in the liver of group C rats. A reduction of body weight was observed in all treatment groups. Cd and Zn were found to be hematoxic and hepatotoxic in the Norwegian rat with Cd exhibiting greater toxicity than Zn. Toxicity of Cd was suppressed by Zn only when both metals were admistered at the same time, but a delay in intake of Zn (after 48 h) had little effect on Cd toxicity.     

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.     

Acute toxicity of ammonia to a freshwater teleost,Labeo bata larvae

Ammonia toxicity tests were performed with Labeo bata (bata) larvae of three different size groups. One hundred percent survival of larvae (500.0?±?4.0?mg) was recorded when exposed to ammonia concentrations of 1.0–13.56?mg?L^?1 at 96?h of exposure. Bata larvae exposed to ammonia concentrations of 15.8–25?mg?L^?1 showed 10–74% mortalities. The 96?h LC₅₀ value for 200 (±5), 250 (±2) and 500 (±4) mg bata larvae were 11.5, 16.8 and 22.5?mg?L^?1 un-ionised ammonia concentrations, respectively. When fish were exposed to different doses of ammonia, behavioural changes immediately occurred even at the lowest dose. At first, the fish became hyperexcitable, the skin darkened and they showed an increased ventilation frequency, fish behaviour became normal, 24?h after exposure. A 96?h LC₅₀ value of un-ionised ammonia showed direct relationship with the increasing size of bata larvae.     

Acute toxicity bioassay using Paramecium caudatum,a key member to study the effects of monocrotophos on swimming behaviour,morphology and reproduction

The toxic effects of an organophosphorous insecticide, monochrotophos (MCP) were investigated on Paramecium caudatum in static acute toxicity tests (10?min and 2?h). The lethal concentrations (50%) were determined by probit method, for technical monocrotophos as 60 and 40.6?mg?L^?1, respectively. We have combined conventional light microscopy and a computerized video tracking system to determine behavioural and morphological changes in paramecium on exposure to MCP. Paramecia exposed to highest concentrations (90–100?mg?L^?1) used for 10?min exposure, exhibited initial increase with subsequent decrease in mobility with enormous blebbing, leading to lysis of cells. In the second set of experiments, the cells exposed to lethal concentration (40.6?mg?L^?1) for 2?h were under stress, and reduced their locomotor behaviour, i.e. distance travelled per unit time (mm in 6?min) and swimming speed (mm?s^?1) with increased time of exposure. In the third set of experiments, the number of generations and generation time in 24?h was evaluated with respect to the different sub lethal concentrations (5, 10, 15 and 20?mg?L^?1) of toxicant. The number of generations decreased and generation time extended significantly in a concentration dependent manner. The results indicate that the Paramecium toxicity assay could be used as a complimentary system to rapidly elucidate the cytotoxic potential of insecticides.     

PFOS青春期暴露对成年期雄性大鼠的生殖毒性

为探究青春期的PFOS暴露对成年后的SD大鼠的生殖毒性,对出生后第21天(PND21)的SD大鼠经口灌胃不同剂量的PFOS(5、10和20mg·kg~(-1)),连续染毒7d,在出生后第56天(PND56)时,对各染毒组SD大鼠的体质量、精子数量、血清中的睾酮浓度,以及睾丸间质细胞睾酮合成的相关基因mRNA水平进行了检测。结果显示,10mg·kg~(-1)剂量组大鼠体质量较对照组明显下降(P<0.01);精子数量在10mg·kg~(-1)和20mg·kg~(-1)剂量组明显降低(P<0.05);血清中睾酮浓度随着PFOS剂量的加大有明显下降的趋势,20mg·kg~(-1)剂量组显著低于对照组(P<0.05);类/胆固醇相关基因star和cyp11α1的mRNA表达水平明显下调。研究表明,青春期的PFOS暴露会导致睾酮合成途径中相关因子的功能缺失,破坏成熟睾丸间质细胞的功能,致使睾酮水平降低,并抑制精子生成,从而破坏生殖系统的功能。     

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.     

A comparitive study between the coal-biomass briquette and raw coal in SO2 pollution and adverse effects in rabbits

This study was conducted to evaluate the adverse health effects on rabbits exposed to SO₂ emitted indoors from burning coals, and compare differences between coal-biomass briquette (B.B.) and raw coal (R.C.). Thirty-six male rabbits were divided equally into three groups at random, and then exposed to burning R.C., B.B., and the third without burning coal (Control) for 90 days. Data showed that the average concentration of SO₂ in 24?h in R.C. was 13.04?mg?m^?3, which was 5-fold greater than B.B. (2.68?mg?m^?3) and 31-fold higher than control (0.41?mg?m^?3). After 45 days, the numbers of rabbits, with increased frequency of Comet cell was highest in R.C. After 90 days, the % positive Comet cell was significant at 10.36% in R.C., 5.42% in B.B., and 1.73% in Control. There was a nonlinear dose–effect relationship between % positive Comet cell and the concentration of SO₂. The incidence of interstitial pneumonia was 6/12 in R.C. and 4/12 in B.B. showing severe squamous metaplasia with atypical hyperplasia in bronchial epithelia in R.C. animals. The results of study indicate that use of B.B. reduced the emission of SO₂; but the smoke emitted from burning coal still produced DNA damage.     

Toxic responses of different organs following occupational exposure to sub-threshold limit value levels of paving asphalt fumes

The main purpose of this study was to ascertain whether occupational exposure to asphalt fumes, under normal working conditions, is associated with any hepatotoxic, nephrotoxic, or hematotoxic response. This was a cross-sectional study in which 210 subjects (80 exposed and 130 reference subjects) were investigated. Using standard methods, atmospheric concentrations of total particulate and benzene-soluble fractions of asphalt fumes were measured. Additionally, urine and blood samples were taken from subjects for complete blood count, white blood cell differential test, urinalysis, and routine biochemical tests of kidney and liver function. Both groups were similar as far as their demographic variables and smoking habits were concerned. The levels of exposure to total particulate and benzene-soluble fractions were estimated to be 0.9?±?0.2 and 0.32?±?0.09 mg m^?3, respectively (mean?±?SD), both of which being lower than the existing threshold limit values. Statistically, significant associations between exposure to asphalt fumes and changes in most liver and kidney function tests and complete blood count parameters provided circumstantial evidence in favor of the notion that exposure to sub-threshold limit value levels of total particulate and benzene-soluble fractions is associated with early liver and kidney dysfunction as well as hematological disorders.     

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.     

Acute toxicity of benzophenone-type UV filters and paraben preservatives to freshwater planarian,Dugesia japonica

Fourteen benzophenone-type UV filters and four paraben preservatives were selected to examine their acute toxicities on Dugesia japonica. The 48-h LC₅₀ values for planarians exposed to benzophenone-type UV filters can be ranked as oxybenzone?>?mexenone?>?5-chloro-2-hydroxybenzophenone?> 2,4-dihydroxybenzophenone?>?2-hydroxybenzophenone?>?dioxybenzone?>?benzophenone?>?2,2′,4,4′-tetrahydroxybenzophenone?>?4-hydroxybenzophenone?> 3-hydroxybenzophenone?>?4,4′-dihydroxybenzophenone?>?2,2′-dihydroxy-4,4′-dimethoxybenzophenone?>?2,3,4-trihydroxybenzophenone?>?sulisobenzone with a range from 0.9 to 145?mg?L^?1 with a similar sequence for the 96?h LC₅₀ values, ranging from 0.5 to 77?mg?L^?1. The 48 and 96?LC₅₀ values for planarians exposed to paraben preservatives can be ranked as butylparaben?>?propylparaben?>?ethylparaben?>?methylparaben. Among all the tested chemicals, oxybenzone was the most toxic and sulisobenzone the least toxic chemical to planarian at each exposure period. Most benzophenone-type UV filters are toxic to aquatic animals with 48?h LC₅₀ values less than 10 mg?L^?1, except for 2,2′-dihydroxy-4,4′-dimethoxybenzophenone, 2,3,4-trihydroxybenzophenone, and sulisobenzone. Because of their common occurrence in aquatic environment, more studies on aquatic toxicities of benzophenone-type UV filters and paraben preservativs are needed to provide important information to adequately assess their ecological risk.