Effects of dietary uranium on reproductive endpoints--fecundity, survival, reproductive success--of the fish Danio rerio

Exposure to metal-contaminated water has been shown to result in a number of reproductive abnormalities in adult and larvae fish, such as failure of oocyte maturation and teratogenic effects. Recently, dietary uptake of metals by fish has been recognized as a critical route of exposure, however, the mechanisms of metal uptake and toxicity are poorly understood and in need of further investigation. The objectives of the present study are to quantify uranium (U dietary transfers from spiked artificial diets) in Danio rerio tissues and embryos, as well as establish its effect on reproduction and embryonic development. Uranium's environmental prominence is currently increasing because of new mining and milling activities. Uranium concentrations range from 0.02?μg/L in natural waters to 2?mg/L. The focus of this study was to examine the trophic transfer and effects of U following exposure modalities (dose, exposure duration 1 to 20 d). Two different isotopes were used to distinguish between chemical and radioactivity toxicity of U. Results showed that U trophic transfer was low (0.52%). Uranium tissue distributions showed that accumulation occurred in digestive organs (liver, digestive tract) following dietary exposure. High levels of U were measured in the gonads (female in particular, >20% of relative burden). High U accumulation levels in eggs indicated maternal transfer of the contaminant. Moreover, U trophic exposure led to a reduction in reproduction success as a function of U accumulated levels. High U exposure conditions strongly reduced the total number of eggs (50%) and their viability at 10 d (reduction of the clutch number, low quality of eggs).     

Toxicity of Cadmium-Contaminated Clay to the Zebrafish Danio rerio

In this study, the toxicity of cadmium-contaminated clay to the zebrafish Danio rerio was evaluated. Kaolin clay was spiked with CdCl₂ (1.28 mg Cd/g clay) and adult zebrafish were exposed to 0, 500, 1,000, and 2,000 mg/L Cd-contaminated clay in a continuous recirculation system. Cumulative mortality was evaluated as a function of exposure time, and LT50 values were calculated. Results of acute toxicity tests showed that an exposure to 1,000 mg/L Cd-contaminated clay resulted in LT50 values of 12 and 92 h (n = 2 experiments) and in a LT50 value of 22 h in both experiments with 2,000 mg/L Cd-contaminated clay. Positive control experiments with corresponding measured dissolved Cd concentrations were performed to evaluate by comparison the toxicity of the clay-bound Cd. These control experiments gave LT50 values higher than 144 h for both conditions. Moreover, no toxicity (LT50 > 144 h) of 2,000 mg/L uncontaminated clay was observed. This study showed that cadmium present on clay particles can be bioavailable and exert a toxic effect to the zebrafish D. rerio. Received: 26 January 1999/Accepted: 12 July 1999     

Hydroxyl radical generation and oxidative stress in Carassius auratus liver, exposed to pyrene

This paper studied the hydroxy radical generation and oxidative stress in the liver of goldfish Carassius auratus under the effect of pyrene. Fish were exposed to different concentrations (0.001, 0.005, 0.01, 0.05 and 0.1 mg/L) of pyrene for 10 days, with one group assigned as control. Based on the hyperfine splitting constants and shape of the electron paramagnetic resonance (EPR) spectrum, the free radical which was generated in fish liver was identified as hydroxyl radical ((*)OH). The (*)OH signal intensity showed a significant increase compared with the control. The changes of the activities of catalase (CAT), superoxide dismutase (SOD), and glutathione-S-transferase (GST) were detected. The reduced glutathione (GSH) level decreased significantly while oxidized glutathione (GSSG) level was increased at higher concentration (0.005-0.1 mg/L), resulting in a decreased GSH/GSSG ratio, and the malondialdehyde (MDA) content increased significantly at 0.005-0.1 mg/L pyrene. The results clearly showed that C. auratus was subjected to oxidative stress and damage when exposed to pyrene.     

Reproductive impairment in the zebrafish, Danio rerio, upon chronic exposure to 1,2,3-trichlorobenzene

Most organic pollutants are supposed to act via the mechanism of nonpolar narcosis upon acute exposure. Because the chronic effects of these compounds are still relatively unknown, in this study a chronic toxicity experiment was performed with zebrafish, Danio rerio, exposed to 1,2,3-trichlorobenzene (123TCB), a nonpolar narcotic. Fish were exposed in a flow-through system for 68 and 147 days. Parameters measured are survival, growth, reproduction, and glycogen and protein content. The only parameter which was influenced was the number of eggs produced per female, resulting in an EC(50) of 40 microg/L. Using this value and acute toxicity data for 123TCB, an acute to chronic ratio (ACR) of 80 was calculated, which is larger than ACRs for other species exposed to nonpolar narcotics. This finding might indicate that compounds acting by nonpolar narcosis in acute tests can have completely different effects upon chronic exposure.     

Concentration-response concept in ecotoxicoproteomics: effects of different phenanthrene concentrations to the zebrafish (Danio rerio) embryo proteome

Concentration-response experiments, based on the testing of less replicates in favour of more exposure concentrations, represent the typical design of choice applied in toxicological and ecotoxicological effect assessment studies using traditional endpoints such as lethality. However, to our knowledge this concept has not found implementation in the increasingly applied OMICS techniques studying thousands of molecular endpoints at the same time. The present study is among the first applying the concentration-response concept for an ecotoxicoproteomics study. The effects of six different concentrations in the low effect range (相似文献   

Evidence of oxidative stress in American kestrels exposed to electromagnetic fields.

Exposure to electromagnetic fields (EMFs) alters melatonin, behavior, growth, and reproduction of captive American kestrels (Falco sparverius), particularly of males. EMF exposure is a "possible" human carcinogen and associated with some neurodegenerative diseases. Oxidative stress contributes to cancer, neurodegenerative diseases, and immune disorders. We tested whether EMF exposure elicits an avian immune response and alters oxidative stress levels. Captive male kestrels were bred under control or EMF conditions equivalent to those experienced by wild kestrels. Short-term EMF exposure (one breeding season) suppressed plasma total proteins, hematocrits, and carotenoids in the first half of the breeding season. It also suppressed erythrocyte cells and lymphocyte proportions, but elevated granulosa proportions at the end of the breeding season. Long-term EMF exposure (two breeding seasons) suppressed hematocrits in the first half of the reproductive period too. Results indicate that only short-term EMF birds experience an immune response, particularly during the early half of the breeding season. The elevation of granulocytes, and the suppression of carotenoids, total proteins, and previously melatonin in the same kestrels, signifies that the short-term EMF male kestrels had higher levels of oxidative stress, due to an immune response and/or EMF exposure. Long-term EMF exposure may be linked to higher levels of oxidative stress through EMF exposure only.     

Enhanced oxidative stress and endothelial dysfunction in streptozotocin-diabetic rats exposed to fine particles

The association between ambient particulate matter (PM) and cardiovascular diseases has been demonstrated in epidemiological studies. Recent studies suggest that diabetic patients are at greater risk for PM-associated cardiovascular events. Although diabetes and PM exposure individually have been reported to be associated with increased oxidative stress, inflammation, and endothelial dysfunction, it is not clear whether PM may induce synergistic interaction effects on these parameters in diabetics. Strepotozotocin-induced diabetic (n=4) and healthy (n=4) rats were intratracheally administered with PM2.5 collected from a busy traffic area in a dose of 200 microg suspended in 0.5 mL phosphate-buffered saline (PBS). The same number of rats was exposed to PBS as controls. Cell and differential counts and protein and lactate dehydrogenase activity were determined in bronchoalveolar lavage. Markers of 8-hydroxydeoxy-guanosine (8-OHdG), endothelin-1 (ET-1), and [nitrate+nitrite], an indicator of nitric oxide (NO) production, in addition to C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) in peripheral blood were also determined. Our results showed that diabetic rats were associated with increased 8-OHdG, IL-6, and ET-1 decreased [nitrate+nitrite]. In nondiabetic rats PM exposure was also associated with increased 8-OHdG, IL-6, TNF-alpha, and CRP but decreased [nitrate+nitrite]. Interestingly, increases of 8-OHdG and ET-1 after PM exposure were more prominent in diabetic rats than in nondiabetic rats. The general linear model further indicated that there were interactions between diabetes and PM on 8-OHdG (P<0.01) and ET-1 (P=0.08). We suggest that PM exposure may enhance the risk of cardiovascular diseases through interaction between PM and diabetes on excess reactive oxygen species generation and endothelial dysfunction. These findings provide further support for previous epidemiological studies.     

Aluminum-induced oxidative stress and neurotoxicity in grass carp (Cyprinidae--Ctenopharingodon idella)

Aluminum is used in a large number of anthropogenic processes, leading to aquatic ecosystems pollution. Diverse studies show that in mammals this metal may produce oxidative stress, is neurotoxic, and is involved in the development of neurodegenerative disorders, such as Alzhaimer's and Parkinson's diseases. Nevertheless, there are only few studies with respect to Al-induced neurotoxicity on aquatic fauna, particularly on fishes of economical interest, such as the grass carp (Ctenopharingodon idella). This study evaluates Al-induced toxicity on the grass carp C. idella. Specimens were exposed to the maximum concentration allowed in order to protect aquatic life (0.1 mg L?1), for 12, 24, 48, 72 and 96 h. After the exposure time, lipid peroxidation degree, superoxide dismutase and catalase activity, as well as dopamine, adrenaline and noradrenaline levels were evaluated. Al concentration in organisms and water was also measured, in order to determine the bioconcentration factor. Results show that Al bioconcentrates in grass carp inducing oxidative stress (increment of 300 and 455 percent on lipid peroxidation degree and SOD activity, and decrement of 49 percent on CAT activity) and neurotoxicity (increment of 55 and 155 percent on dopamine and adrenaline levels and decrement of 93 percent on noradrenaline level).     

Joint toxicity of sodium arsenate and sodium perchlorate to zebrafish Danio rerio larvae

Joint toxicity of arsenate and perchlorate was tested in larvae of Danio rerio. Results indicated that the 96-h median lethal concentrations of sodium arsenate and sodium perchlorate were 258.8 and 1,401.2 mg/L, respectively, and that arsenate and perchlorate generally showed a concentration-additive effect.     

Standardized Bacopa monnieri extract ameliorates acute paraquat-induced oxidative stress,and neurotoxicity in prepubertal mice brain

Objectives: Bacopa monnieri (BM), an ayurvedic medicinal plant, has attracted considerable interest owing to its diverse neuropharmacological properties. Epidemiological studies have shown significant correlation between paraquat (PQ) exposure and increased risk for Parkinson's disease in humans. In this study, we examined the propensity of standardized extract of BM to attenuate acute PQ-induced oxidative stress, mitochondrial dysfunctions, and neurotoxicity in the different brain regions of prepubertal mice.

Methods: To test this hypothesis, prepubertal mice provided orally with standardized BM extract (200?mg/kg body weight/day for 4 weeks) were challenged with an acute dose (15?mg/kg body weight, intraperitoneally) of PQ after 3 hours of last dose of extract. Mice were sacrificed after 48 hours of PQ injection, and different brain regions were isolated and subjected to biochemical determinations/quantification of central monoamine (dopamine, DA) levels (by high-performance liquid chromatography).

Results: Oral supplementation of BM for 4 weeks resulted in significant reduction in the basal levels of oxidative markers such as reactive oxygen species (ROS), malondialdehyde (MDA), and hydroperoxides (HP) in various brain regions. PQ at the administered dose elicited marked oxidative stress within 48 hours in various brain regions of mice. However, BM prophylaxis significantly improved oxidative homeostasis by restoring PQ-induced ROS, MDA, and HP levels and also by attenuating mitochondrial dysfunction. Interestingly, BM supplementation restored the activities of cholinergic enzymes along with the restoration of striatal DA levels among the PQ-treated mice.

Discussion: Based on these findings, we infer that BM prophylaxis renders the brain resistant to PQ-mediated oxidative perturbations and thus may be better exploited as a preventive approach to protect against oxidative-mediated neuronal dysfunctions.     

Food deprivation exacerbates mitochondrial oxidative stress in rat liver exposed to ischemia-reperfusion injury

Mitochondria undergo oxidative damage during reperfusion of ischemic liver. Although nutritional status affects ischemia-reperfusion injury in the liver, its effect on mitochondrial damage has not been evaluated. Thus, this study was designed to determine whether starvation influences the oxidative balance in mitochondria isolated from livers exposed to warm ischemia-reperfusion. Fed and 18- and 36-h food-deprived rats underwent partial hepatic ischemia followed by reperfusion. Mitochondria were isolated before and after ischemia and during reperfusion. Serum alanine transaminase was measured to assess liver injury. The mitochondrial concentrations of malondialdehyde, protein carbonyls and glutathione were determined as indicators of oxidative injury. Cell ultrastructure was assessed by transmission electron microscopy. Transaminase levels were greater in 18-h food-deprived than fed rats (after 120 min of reperfusion: 3872 +/- 400 vs. 1138 +/- 59 U/L, P < 0.01). Mitochondrial glutathione was lower in food-deprived than fed rats before and after ischemia, and during reperfusion. Food deprivation also was associated with significantly greater lipid and protein oxidative damage. Finally, more ultrastructural damage was observed during reperfusion in mitochondria from food-deprived rats. Prolonging the length of food deprivation to 36 h exacerbated significantly both the mitochondrial oxidative injury and the release of serum transaminases in rats (after 120 min of reperfusion: 5438 +/- 504 U/L, P < 0.01). Food deprivation was associated with greater mitochondrial oxidative injury in rat livers exposed to warm ischemia-reperfusion, and the extent of oxidative damage in mitochondria increased with the length of food deprivation.     

Electroencephalogram, cognitive state, psychological disorders, clinical symptom, and oxidative stress in horticulture farmers exposed to organophosphate pesticides

The aim of this paper was to study the toxicity of organophosphate (OP) pesticides in exposed farmers for electroencephalography, cognitive state, psychological disorders, clinical symptom, oxidative stress, acetylcholinesterase, and DNA damage. A comparative cross-sectional analysis was carried out in 40 horticulture farmers who were exposed to OPs in comparison to a control group containing 40 healthy subjects with the same age and sex and education level. Lipid peroxidation (LPO), superoxide dismutase (SOD), catalase, glutathione peroxidase, DNA damage, total antioxidant capacity (TAC), total thiol molecules, and acetylcholinesterase (AChE) activity were measured in the blood of subjects. Clinical examination and complete blood test were undertaken in order to record any abnormal sign or symptoms. Cognitive function, psychological symptoms, and psychological distress were examined and recorded. Comparing with controls, the farmers showed higher blood levels of SOD and LPO while their TAC decreased. Farmers showed clinical symptoms such as eczema, breathing muscle weakness, nausea, and saliva secretion. Regarding cognitive function, the orientation, registration, attention and calculation, recall, and language were not significantly different in farmers and controls. Among examinations for psychological distress, only labeled somatization was significantly higher in farmers. The present findings indicate that oxidative stress and inhibition of AChE can be seen in chronically OP-exposed people but incidence of neuropsychological disorders seems a complex multivariate phenomenon that might be seen in long-term high-dose exposure situations. Use of supplementary antioxidants would be useful in the treatment of farmers.     

长期铅暴露雄性大鼠脑组织铁过载及DNA氧化损伤

目的 研究铅暴露对不同生长阶段SD雄性大鼠脑组织铅、铁水平及DNA氧化损伤的影响.方法 将12只SPF级SD雌性大鼠随机分为3组,分别为空白对照(去离子水)组和低(0.8 g/L)、高(1.5 g/L)剂量乙酸铅染毒组,每组4只.采用自由饮水方式进行染毒,自妊娠前10d至仔鼠断乳(出生后21d).待断乳后,每组选取21只雄性仔鼠,相应各组分别自由饮用去离子水和0.3、0.9 g/L乙酸铅溶液.仔鼠分别饲养至断乳(21d)、中年(12个月)、老年(18个月)时,检测脑组织中铅、铁和8-羟基脱氧鸟苷(8-hydroxy-2'-deoxyguanosine,8-OHdG)的水平.结果 在同一生长阶段,随着铅染毒剂量的升高,大鼠脑铅、脑铁及脑组织8-OHdG水平均增加.线性回归分析结果显示,在断乳期和老年期,大鼠脑铁、脑8-OHdG水平随着脑铅水平的升高而上升(P＜0.05);同时,脑铅、脑铁联合作用使大鼠脑8-OHdG水平升高(P＜0.05).而中年期无明显改变.在空白对照组和各剂量铅染毒组中,随着铅染毒时间的延长,大鼠脑铅、脑铁水平均增高(P＜0.05).空白对照组中,脑8-OHdG水平在中年、老年期增高(P＜0.05);低剂量组改变不明显;高剂量组在老年期明显升高(P＜0.05),中年期改变不明显.结论 铅暴露可致SD大鼠脑组织铁过载及DNA氧化损伤.     

外源性谷胱甘肽对慢性砷暴露小鼠尿砷代谢及氧化应激的影响

目的探讨给与谷胱甘肽(GSH)及其拮抗剂——丁硫氨酸亚砜胺(BSO)对慢性砷暴露小鼠体内砷代谢及氧化应激的影响。方法将SPF级雌性昆明小鼠随机分为对照组(蒸馏水)、单纯染砷组(50 mg/L亚砷酸钠)、GSH干预组(50 mg/L亚砷酸钠+400 mg/kg GSH)和BSO(50 mg/L亚砷酸钠+600mg/kg BSO)干预组,除对照组小鼠饮用蒸馏水外,其余各组均饮用含50 mg/L亚砷酸钠的水溶液连续染毒30周,然后给予400 mg/kg GSH或600 mg/kg BSO,用蒸馏水配制GSH和BSO水溶液,每天两次腹腔注射,连续2 d,用氢化物发生-超低温捕集-原子吸收分光光度法测定尿液各形态砷水平,用DTNB及试剂盒法分别测定全血及肝脏中GSH和总抗氧化能力(T-AOC)水平。结果 GSH干预组小鼠尿中二甲基胂(DMA)、DMA含量构成比、二甲基化率(SMR)及总砷含量高于单纯染砷组(P<0.05),而BSO干预组各形态砷、DMA含量构成比、一甲基化率(FMR)、SMR及总砷含量均低于单纯染砷组(P<0.05);单纯染砷组小鼠肝脏和血液GSH和T-AOC的水平均低于对照组(P<0.05)。给予GSH干预后,肝脏和血液GSH和T-AOC水平均高于单纯染砷组(P<0.05)且与对照组差异无统计学意义(P>0.05)。BSO干预组小鼠肝脏和血液GSH和T-AOC的水平均低于其他各组(P<0.05)。结论外源性GSH干预可以增强砷暴露小鼠的砷甲基化能力,增加砷从尿液中的排出,拮抗砷所致的GSH和T-AOC水平下降,从而减少了砷对机体造成的氧化损伤。     

番茄红素对氟染毒小鼠氧化应激及行为影响

目的 探讨番茄红素对饮水性氟染毒小鼠氧化应激损伤与神经行为影响及可能机制。方法 成年雄性C57BL/6小鼠60只,随机分为对照组、染氟组、番茄红素组、番茄红素低、中、高剂量干预组,每组10只;连续处理6个月后, 氟离子选择电极法测定尿氟、血氟和脑氟含量;化学比色法检测血液和海马组织中丙二醛(MDA)含量及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶(CAT)活力;水迷路实验分析小鼠神经行为学改变。结果 与对照组比较,染氟组小鼠体重下降,尿氟、血氟和脑氟含量[分别为(3.76±1.60)、(19.26±0.62)、(1.19±0.12) mg/kg]升高(P<0.05),血液和海马组织中MDA含量显著增加、SOD、GSH-Px和CAT 酶活力下降(P<0.05);与染氟组比较,番茄红素高剂量干预组尿氟、血氟和脑氟含量[分别为(2.06±0.47)、(13.40±0.35)、(0.52±0.21) mg/kg]明显下降(P<0.05),血液和海马组织中MDA含量降低、SOD、GSH-Px和CAT 酶活力升高(P<0.05);与对照组比较,染氟组小鼠平均逃逸时间和靶象限活动时间[分别为(20.84±0.72)、(16.11±0.77) s]延长(P<0.05);与染氟组比较,番茄红素高剂量干预组小鼠平均逃逸时间和靶象限活动时间[分别为(14.01±0.82)、(7.38±0.37) s]下降(P<0.05)。结论 番茄红素能有效降低饮水性氟染毒小鼠氧化应激损伤及提高小鼠学习记忆能力,对饮水性氟中毒具有一定保护作用。