Environmental profiles for the selected metals were compiled on the basis of available data on their biological activities. Analysis of the profiles suggests that the concept of toxic heavy metals and safe nontoxic alternatives based on lighter metals should be re-evaluated. Comparison of the toxicological data indicates that palladium, platinum, and gold compounds, often considered heavy and toxic, may in fact be not so dangerous, whereas complexes of nickel and copper, typically assumed to be green and sustainable alternatives, may possess significant toxicities, which is also greatly affected by the solubility in water and biological fluids. It appears that the development of new catalysts and novel applications should not rely on the existing assumptions concerning toxicity/nontoxicity. Overall, the available experimental data seem insufficient for accurate evaluation of biological activity of these metals and its modulation by the ligands. Without dedicated experimental measurements for particular metal/ligand frameworks, toxicity should not be used as a "selling point" when describing new catalysts.

Which Metals are Green for Catalysis? Comparison of the Toxicities of Ni, Cu, Fe, Pd, Pt, Rh, and Au Salts.

The major pesticides of the world are glyphosate-based herbicides (GBH), and their toxicity is highly debated. To understand their mode of action, the comparative herbicidal and toxicological effects of glyphosate (G) alone and 14 of its formulations were studied in this work, as a model for pesticides. GBH are mixtures of water, with commonly 36-48% G claimed as the active principle. As with other pesticides, 10-20% of GBH consist of chemical formulants. We previously identified these by mass spectrometry and found them to be mainly families of petroleum-based oxidized molecules, such as POEA, and other contaminants. We exposed plants and human cells to the components of formulations, both mixed and separately, and measured toxicity and human cellular endocrine disruption below the direct toxicity experimentally measured threshold. G was only slightly toxic on plants at the recommended dilutions in agriculture, in contrast with the general belief. In the short term, the strong herbicidal and toxic properties of its formulations were exerted by the POEA formulant family alone. The toxic effects and endocrine disrupting properties of the formulations were mostly due to the formulants and not to G. In this work, we also identified by mass spectrometry the heavy metals arsenic, chromium, cobalt, lead and nickel, which are known to be toxic and endocrine disruptors, as contaminants in 22 pesticides, including 11 G-based ones. This could also explain some of the adverse effects of the pesticides. In in vivo chronic regulatory experiments that are used to establish the acceptable daily intakes of pesticides, G or other declared active ingredients in pesticides are assessed alone, without the formulants. Considering these new data, this assessment method appears insufficient to ensure safety. These results, taken together, shed a new light on the toxicity of these major herbicides and of pesticides in general.

Toxicity of formulants and heavy metals in glyphosate-based herbicides and other pesticides

In the last two decades, nanotechnologies demonstrated various applications in different fields, including detection, sensing, catalysis, electronics, and biomedical sciences. However, public concerns regarding the well-being of human may hinder the wide utilization of this promising innovation. Although humans are exposed to airborne nanosized particles from an early age, exposure to such particles has risen dramatically within the last century due to anthropogenic sources of nanoparticles. The wide application of nanomaterials in industry, consumer products, and medicine has raised concerns regarding the potential toxicity of nanoparticles in humans. In this review, the effects of nanomaterials on the reproductive system in animal models are discussed. Females are particularly more vulnerable to nanoparticle toxicity, and toxicity in this population may affect reproductivity and fetal development. Moreover, various types of nanoparticles have negative impacts on male germ cells, fetal development, and the female reproductive system. These impacts are associated with nanoparticle modification, composition, concentration, route of administration, and the species of the animal. Therefore, understanding the impacts of nanoparticles on animal growth and reproduction is essential. Many studies have examined the effects of nanoparticles on primary and secondary target organs, with a concentration on the in vivo and in vitro effects of nanoparticles on the male and female reproductive systems at the clinical, cellular, and molecular levels. This review provides important information regarding organism safety and the potential hazards of nanoparticle use and supports the application of nanotechnologies by minimizing the adverse effects of nanoparticles in vulnerable populations.

/pdf/toxicity-of-nanoparticles-on-the-reproductive-system-in-4s37tvr0av.pdf

Toxicity of Nanoparticles on the Reproductive System in Animal Models: A Review.

Graphene oxide (GO) has been extensively studied for potential biomedical applications. Meanwhile, potential GO toxicity arises in both biomedical applications and non-biomedical products where environmental exposures may occur. In the present study, we examined the potential adverse effects of GO and the underlying mechanism using nematode Caenorhabditis elegans as the assay system. We compared the in vivo effects of GO between acute exposure and prolonged exposure, and found that prolonged exposure to 0.5-100 mg L(-1) of GO caused damage on functions of both primary (intestine) and secondary (neuron and reproductive organ) targeted organs. In the intestine, ROS production was significantly correlated with the formation of adverse effects on functions of both primary and secondary targeted organs. GO could be translocated into intestinal cells with loss of microvilli, and distributed to be adjacent to or surrounding mitochondria. Prolonged exposure to GO resulted in a hyper-permeable state of the intestinal barrier, an increase in mean defecation cycle length, and alteration of genes required for intestinal development and defecation behavior. Thus, our data suggest that prolonged exposure to GO may cause potential risk to environmental organisms after release into the environment. GO toxicity may be due to the combinational effects of oxidative stress in the intestinal barrier, enhanced permeability of the biological barrier, and suppressed defecation behavior in C. elegans.

Contributions of altered permeability of intestinal barrier and defecation behavior to toxicity formation from graphene oxide in nematode Caenorhabditis elegans

Abstract In the past decades, much attention has been paid to toxicity assessment of nanoparticles prior to clinical and biological applications. While in vitro studies have been increasing constantly, in vivo studies of nanoparticles have not established a unified system until now. Predictive models and validated standard methods are imperative. This review summarizes the current progress in approaches assessing nanotoxicity in main systems, including the hepatic and renal, gastrointestinal, pulmonary, cardiovascular, nervous, and immune systems. Histopathological studies and specific functional examinations in each system are elucidated. Related injury mechanisms are also discussed.

https://www.degruyter.com/downloadpdf/j/ntrev.2017.6.issue-3/ntrev-2016-0047/ntrev-2016-0047.xml

Toxicity assessment of nanoparticles in various systems and organs

Nickel is associated with reproductive toxicity. However, the reproductive toxicity of nickel nanoparticles (Ni NPs) is unclear. Our goal was to determine the association between nickel nanoparticle exposure and reproductive toxicity. According to the one-generation reproductive toxicity standard, rats were exposed to nickel nanoparticles by gavage and we selected indicators including sex hormone levels, sperm motility, histopathology, and reproductive outcome etc. Experimental results showed nickel nanoparticles increased follicle stimulating hormone (FSH) and luteinizing hormone (LH), and lowered etradiol (E2) serum levels at a dose of 15 and 45 mg/kg in female rats. Ovarian lymphocytosis, vascular dilatation and congestion, inflammatory cell infiltration, and increase in apoptotic cells were found in ovary tissues in exposure groups. For male rats, the weights decreased gradually, the ratio of epididymis weight over body weight increased, the motility of rat sperm changed, and the levels of FSH and testosterone (T) diminished. Pathological results showed the shedding of epithelial cells of raw seminiferous tubule, disordered arrangement of cells in the tube, and the appearance of cell apoptosis and death in the exposure group. At the same time, Ni NPs resulted in a change of the reproductive index and the offspring development of rats. Further research is needed to elucidate exposure to human populations and mechanism of actions.

Nickel Nanoparticles Exposure and Reproductive Toxicity in Healthy Adult Rats

Previous studies have not examined the adverse effects of microcystin-LR (MC-LR) at environmental relevant concentrations on the development and functions of nervous system. The neurotoxic effects of MC-LR exposure on neurotransmitter systems were investigated in Caenorhabditis elegans. After exposing L1 larvae to 0.1, 1, 10, and 100 μg l−1 of MC-LR for 8 and 24 h, the adverse effects on GABAergic, cholinergic, serotonergic, dopaminergic, and glutamatergic neurons were examined. The expression levels of genes required for development and functions of GABAergic neurons were further investigated. Body bend frequency and head thrash frequency decreased significantly after MC-LR exposure for 8 h at concentrations more than 1 μg l−1 and after MC-LR exposure for 24 h at concentrations more than 0.1 μg l−1. Loss of GABAergic neurons increased significantly in a dose-dependent manner after MC-LR exposure at concentrations more than 0.1 μg l−1. In contrast, no obvious neuronal losses or morphologic changes were observed in cholinergic, serotonergic, dopaminergic, and glutamatergic neurons in MC-LR-exposed nematodes. Quantitative real-time PCR assay further showed that expression levels of unc-30, unc-46, unc-47, and exp-1 genes required for development and function of GABAergic neurons decreased significantly in nematodes exposed to MC-LR at concentrations more than 0.1 or 1 μg l−1. MC-LR at environmental relevant concentrations caused neurobehavioral defects, which may be largely due to the neuronal loss and the alterations of expression level of genes required for GABAergic neurotransmitter system in C. elegans.

Neurotoxicological evaluation of microcystin-LR exposure at environmental relevant concentrations on nematode Caenorhabditis elegans

Previous studies have revealed that chlorpyrifos exposure adversely affects the reproductive capacity of male rodents. The present study investigated the reproductive toxicity of chlorpyrifos exposure and possible related mechanisms using the nematode Caenorhabditis elegans. L4 nematode larvae were exposed to chlorpyrifos at concentrations of 0.003, 0.03, 0.3 and 3.0 mg l(-1) for different durations. In addition to decreased brood size, reduced spermatid size, increased percentage of abnormal spermatids, suppressed spermatid activation and motility of sperm, damaged oocyte morphology, increased numbers of apoptotic cells and unfertilized oocytes were observed in nematodes exposed to various concentrations of chlorpyrifos. Moreover, expression patterns of the genes spe-10, spe-15, fer-1, prg-1, glp-1, mlh-1, cyb-3, ced-3, ced-4 and ced-9 (which are associated with spermatid size, spermatid activation and morphology, oocyte morphology, oocyte function, and apoptosis) were altered after chlorpyrifos exposure. Therefore, chlorpyrifos exposure may adversely affect fertility in nematodes by influencing both spermatogenesis and oogenesis. Alterations in the expression patterns of genes involved in gametogenesis may explain the corresponding changes in gametogenesis in nematodes exposed to chlorpyrifos. Hence, the model organism Caenorhabditis elegans is recommended for assessment of reproductive toxicity relating to gametogenesis.

Dayong Wang

Papers

Nickel Nanoparticles Exposure and Reproductive Toxicity in Healthy Adult Rats

Neurotoxicological evaluation of microcystin-LR exposure at environmental relevant concentrations on nematode Caenorhabditis elegans

Chlorpyrifos exposure reduces reproductive capacity owing to a damaging effect on gametogenesis in the nematode Caenorhabditis elegans.