Elisavet Renieri

Effect of heavy metals on fish larvae deformities: A review

Heavy metals have been associated with many fish deformities in natural populations and in laboratory produced specimens as well. Deformities in general have devastating effects on fish populations since they affect the survival, the growth rates, the welfare and their external image. Although the embryonic stage in respect to heavy metal exposure has been extensively studied, there is not much information available as to what happens in fish larvae and adults. In the present article, we present the available information on the effect of heavy metals on fish larvae deformities. We also address the need for more research towards the effects of metals on the subsequent life stages in order to assess the long-term consequences of heavy metal poisoning on fish organisms and possibly correlate these consequences with the environmental contamination (use as biomarkers).

Nonlinear responses to waterborne cadmium exposure in zebrafish. An in vivo study

Abstract Cadmium (Cd) has proved to be associated with numerous toxic effects in aquatic organisms via waterborne exposure. With a view to investigate Cd toxicity along a broad spectrum of exposures reaching from environmental to toxic, we employed adult zebrafish (Danio rerio) for an in vivo study. A number of 10 fish per tank were placed in 40 L tanks and were exposed for 30 days to 0.0, 5.0, 25, 50, 75, 100 and 1000 &mgr;g Cd per liter. There were 2 tanks for each Cd exposure (duplicate experiment). Mortality was recorded daily, dead fish were collected and tissue samples were obtained for histologic observation, whereas remaining tissues were stored for Cd burden determination. Surviving fish were collected at the end of the experiment. Median overall survival (OS) in days was found to be 9.0, 11.0, 8.0 and 7.0 for 25 &mgr;g/L, 50 &mgr;g/L, 75 &mgr;g/L and 100 &mgr;g/L respectively, with all of them showing mortality greater than 50%. Remarkably, fish exposed to the highest Cd concentration (1000 &mgr;g/L) survived the longest exhibiting a mean OS of 29.2 days. Cd determination in fish tissue was conducted with an in house ICP‐MS method and levels ranged from 3.1 to 29.1 ng/mg. Log Cd tissue levels were significantly correlated with the log Cd exposure levels (r = 0.535, p < 0.001). The highest Cd burden was determined for fish exposed to 1000 &mgr;g Cd /L (mean = 12.2 ng/mg). Histopathology supported these results. Our findings disclose a deviation in toxic responses through the range of Cd concentrations, leading to nonlinear responses. These differentiated responses, could be linked to hormesis phenomena. Graphical abstract Figure. No Caption available. HighlightsTissue Cd accumulation is dose dependent but not time dependent.Fish exposed to the highest administered exposure survived the longest.Histopathological findings support nonlinear responses.Unanticipated mortality and histopathology responses in zebrafish could be associated to hormesis phenomena.High dose exposure resulting in less adverse effects is attributed to mechanisms stimulated at low doses.

Rapid method for the simultaneous determination of DDTs and PCBs in hair of children by headspace solid phase microextraction and gas chromatography-mass spectrometry (HSSPME/GC-MS).

The purpose of this study was to develop a rapid and cost efficient hair extraction method, using the headspace solid phase microextraction (HSSPME) technique for the simultaneous determination and biomonitoring of 1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane) (DDT) and its isomers/metabolites and polychlorinated biphenyls (PCBs) in hair samples. A total of 72 head hair samples were collected from children living in urban and rural regions of the island of Crete. Two hundred milligrams of hair were digested under alkaline conditions and thermostated for 30 min at 90°C while a 65 µm PDMS/DVB fibre was exposed into the headspace of the vial. Analytical parameters of the method (time of incubation, agitation speed, recovery, precision, accuracy, carry over, matrix effect, linearity, and selectivity) were examined. Recoveries of the DDTs in the spiked hair samples were calculated from 42.3% for opDDD to 87.1% for opDDE, while recoveries for PCB congeners were from 52.6% for PCB138 to 96.6 % for PCB28. The method was applied for the analysis of authentic hair samples. Significant differences (p=0.001) of the burden to total DDTs (sumDDTs) as well as of the frequencies of detection of positive samples (p=0.020) were observed between the examined regions. Moreover, significant differences in the detected concentrations of PCB congeners were observed for PCB52 (p<0.001) and PCB28 (p=0.017) as well for their prevalence between urban and rural regions. Application of HSSPME for the biomonitoring of DDTs and PCBs biomarkers in hair was tested and successfully applied to the analysis of spiked and authentic hair samples. HSSPME was found to be substantially simpler and faster procedure than previous reported sample treatment procedures.

Effects of carbon and silicon nanotubes and carbon nanofibers on marine microalgae Heterosigma akashiwo

ABSTRACT The effect of carbon and silicon nanotubes (CNTs and SiNTs) and carbon nanofibers (CNFs) to microscopic marine algae Heterosigma akashiwo was studied, using algal growth inhibition for 3 days (acute effect) and 7 days (chronic effect) as toxicity endpoints. The criterion of the toxic effect was the statistically significant reduction of the number of algal cells in the exposed samples compared to the control. Samples did not demonstrate toxic effects at doses 1 mg/l and 10 mg/l. CNTs and SiNTs samples at 100 mg/l exhibited both acute and chronic toxic effects. We assume that the main cause of cell death in these samples was related to the mechanical damage of cell integrity. CNFs at concentrations of 100 mg/l did not inhibit algal growth, but cells with irregular shapes were observed, which were not observed after exposure to CNTs and SiNTs. Nickel impurities present in CNFs samples are presumably the main cause of observed cell deformations. Graphical abstract: Figure. No caption available. HighlightsCarbon and silicon nanotubes did not inhibit algal growth up to 10 mg/l.Carbon nanofibers did not inhibit algal growth at 100 mg/l.Cell death of marine alga Heterosigma akashiwo was associated with mechanical damage.Nickel impurities in carbon nanofibers caused irregular shape formation.

Oxidative Stress in Methylmercury-Induced Cell Toxicity

Methylmercury (MeHg) is a hazardous environmental pollutant, which elicits significant toxicity in humans. The accumulation of MeHg through the daily consumption of large predatory fish poses potential health risks, and the central nervous system (CNS) is the primary target of toxicity. Despite well-described neurobehavioral effects (i.e., motor impairment), the mechanisms of MeHg-induced toxicity are not completely understood. However, several lines of evidence point out the oxidative stress as an important molecular mechanism in MeHg-induced intoxication. Indeed, MeHg is a soft electrophile that preferentially interacts with nucleophilic groups (mainly thiols and selenols) from proteins and low-molecular-weight molecules. Such interaction contributes to the occurrence of oxidative stress, which can produce damage by several interacting mechanisms, impairing the function of various molecules (i.e., proteins, lipids, and nucleic acids), potentially resulting in modulation of different cellular signal transduction pathways. This review summarizes the general aspects regarding the interaction between MeHg with regulators of the antioxidant response system that are rich in thiol and selenol groups such as glutathione (GSH), and the selenoenzymes thioredoxin reductase (TrxR) and glutathione peroxidase (Gpx). A particular attention is directed towards the role of the PI3K/Akt signaling pathway and the nuclear transcription factor NF-E2-related factor 2 (Nrf2) in MeHg-induced redox imbalance.

Overview of Cadmium Thyroid Disrupting Effects and Mechanisms

Humans are exposed to a significant number of chemicals that are suspected to produce disturbances in hormone homeostasis. Hence, in recent decades, there has been a growing interest in endocrine disruptive chemicals. One of the alleged thyroid disrupting substances is cadmium (Cd), a ubiquitous toxic metal shown to act as a thyroid disruptor and carcinogen in both animals and humans. Multiple PubMed searches with core keywords were performed to identify and evaluate appropriate studies which revealed literature suggesting evidence for the link between exposure to Cd and histological and metabolic changes in the thyroid gland. Furthermore, Cd influence on thyroid homeostasis at the peripheral level has also been hypothesized. Both in vivo and in vitro studies revealed that a Cd exposure at environmentally relevant concentrations results in biphasic Cd dose-thyroid response relationships. Development of thyroid tumors following exposure to Cd has been studied mainly using in vitro methodologies. In the thyroid, Cd has been shown to activate or stimulate the activity of various factors, leading to increased cell proliferation and a reduction in normal apoptotic activity. Evidence establishing the association between Cd and thyroid disruption remains ambiguous, with further studies needed to elucidate the issue and improve our understanding of Cd-mediated effects on the thyroid gland.