Some volcanic soils like andosols contain short-range order nanoclays (allophane) which build aggregates with a tortuous and fractal microstructure. The aim of the work was to study the influence of the microstructure and mesoporosity of the allophane aggregates on the pesticide chlordecone retention in soils. Our study shows that the allophane microstructure favors pollutants accumulation and sequestration in soils. We put forth the importance of the mesoporous microstructure of the allophane aggregates for pollutant trapping in andosols. We show that the soil contamination increases with the allophane content but also with the mesopore volume, the tortuosity, and the size of the fractal aggregate. Moreover, the pore structure of the allophane aggregates at nanoscale favors the pesticide retention. The fractal and tortuous aggregates of nanoparticles play the role of nanolabyrinths. It is suggested that chlordecone storage in allophanic soils could be the result of the low transport properties (permeability and diffusion) in the allophane aggregates. The poor accessibility to the pesticide trapped in the mesopore of allophane aggregates could explain the lower pollutant release in the environment. (Résumé d'auteur)

The development of saline-alkali lands has contributed to the increasing discharge of alkaline salt-laden wastewater, which poses a threat to aquatic organisms. However, the comprehensive effect of alkaline salt on Microcystis aeruginosa, a harmful cyanobacterium, remains unclear. In this study, the growth, physiology, cell ultrastructure and production of microcystin-LR (MC-LR) in Microcystis aeruginosa exposed to four levels of alkaline salt stress were evaluated. The growth of Microcystis aeruginosa was stimulated at an electrical conductivity (EC) of 2.5 mS/cm compared to the control, as supported by the increased cell density, photosynthetic pigment and protein contents. Microcystis aeruginosa could tolerate a certain level of alkaline salt (i.e., EC of 5 mS/cm) via increasing photosynthetic pigment contents to protect cells from alkaline salt stress, but the antioxidant defence system and cell ultrastructure were not affected. When EC increased to 7.5 mS/cm, alkaline salt caused oxidative stress and toxicity in Microcystis aeruginosa, as evidenced by analysis of the integrated biomarker response (IBR). Furthermore, the photosynthetic pigment and protein contents decreased, and cell apoptosis associated with ultrastructural changes was observed. Therefore, we propose that EC of 7.5 mS/cm is a threshold for growth of Microcystis aeruginosa. Additionally, the intracellular MC-LR content was stimulated by alkaline salt, and the highest value was observed at EC of 2.5 mS/cm. The extracellular MC-LR content increased with the increasing alkaline salt concentration. When EC was 7.5 mS/cm, the extracellular MC-LR content was significantly higher than in the control and was associated with the upregulated mcyH gene. This study recommends that more attention should be paid to the risk of Microcystis aeruginosa bloom and microcystin-LR pollution in lakes located in salinization regions.

Pharmacologically active compounds found in reclaimed wastewater irrigation or animal manure fertilizers pose potential risks for agriculture. The mechanism underlying the effects of ketoprofen on rice (Oryza sativa L.) seedlings was investigated. The results showed that low concentrations (0.5 mg L⁻¹) of ketoprofen slightly stimulate growth of rice seedlings, while high concentrations can significantly inhibit growth by reducing biomass and causing damage to roots. Ketoprofen affects photosynthetic pigment content (Chla, Chlb, and carotenoids) and chlorophyll synthesis gene (HEMA, HEMG, CHLD, CHLG, CHLM, and CAO) expression. Fluorescence parameters such as minimum fluorescence (F₀), maximum fluorescence (Fₘ), variable fluorescence (Fᵥ), potential photosynthetic capacity (Fᵥ/F₀), maximum quantum efficiency of PSII photochemistry (Fᵥ/Fₘ), electron transfer rate (ETR), and Y(II), Y(NPQ), Y(NO) values were affected, showing photosynthetic electron transfer was blocked. Active oxygen radical (O₂•−and H₂O₂), malondialdehyde and proline content increased. Superoxide dismutase, catalase and ascorbate peroxidase activities, glutathione content and antioxidant-related gene (FSD1, MSD1, CSD1, CSD2, CAT1, CAT2, CAT3, APX1, APX2) expression were induced. Higher integrated biomarker response values of eight oxidative stress response indexes were obtained at higher ketoprofen concentrations. Ultrastructure observation showed that ketoprofen causes cell structure damage, chloroplast swelling, increase in starch granules, and reduction in organelles. This study provides some suggested toxicological mechanisms and biological response indicators in rice due to stress from pharmacologically active compounds.

Glandless cotton can be grown to obtain cotton seeds free of toxic gossypol for use as both food and feed. However, they are not grown normally due to their lesser productivity and higher susceptibility to biotic stress. Great attention has been paid to biotic stresses rather than abiotic stresses on glandless cotton. Chromium (Cr) is a common pollutant of soil and considered a serious threat to plants due to its adverse effects on different functions. Although numerous studies are available on the toxicity of Cr⁶⁺ in various plants. However, its adverse effects and mechanism of toxicity in glandless cotton can seldom be found in the literature. This study examined the Cr⁶⁺ effect on glandless cotton in comparison to glanded cotton. Four pairs of glanded and glandless cotton near-isogenic lines (NILs) were exposed to different doses (0, 10, 50, and 100 μM/L) of Cr⁶⁺ for seven days, and biochemical, physiological, molecular, and ultrastructure changes were observed, which were significantly affected by Cr⁶⁺ at high concentrations in all NILs. The effect of Cr⁶⁺ on ionic contents shows the same trend in glanded and glandless NILs except for manganese (Mn²⁺) that show inhibition in glandless (ZMS-12w and Coker-312w) and enhance in the glanded NIL (ZMS-17). The gene expression of superoxide dismutase (SOD) and peroxidase (POD) revealed similar trends as enzyme activities in glandless NILs. The principal component analysis (PCA) and Agglomerative hierarchical clustering (AHC) results of all NILs from morpho-physiological traits, cluster ZMS-16, and ZMS-17 into Cr⁶⁺ sensitive group. While the glandless NILs have the potential to cope with the Cr toxicity by increasing the antioxidant enzyme activity and their gene expression. This study also revealed that Cr⁶⁺ tolerance in cotton is genotypic and has an independent mechanism in the root that not related to low gossypol.

T-2 toxin is an unavoidable contaminant in human food, animal feeds, and agricultural products. T-2 toxin has been found to impair male reproductive function. But, few data is available that reveals the reproductive toxicity mechanism. In the study, male Kunming mice were orally administrated with T-2 toxin at the doses of 0, 0.5, 1 or 2 mg/kg body weight for 28 days. The body and reproductive organs weight, the concentration, malformation rate and ultrastructure of sperm in cauda epididymis were detected. Oxidative stress biomarkers and apoptosis were also measured in testes. Histological change of testes was performed by H&E and TUNEL staining. T-2 toxin down-regulated body and reproductive organs (testis, epididymis and seminal vesicle) weight, sperm concentration, increased sperm malformation rate and damaged the ultrastructure of sperm and structure of testes. T-2 toxin treatment increased the reactive oxygen species (ROS) and malondialdehyde content, while, decreased the total anti-oxidation capacity (T-AOC) and the superoxide dismutase activity in testes. T-2 toxin exposure increased the TUNEL-positive germ cells, the activities and mRNA expressions of caspase-3, caspase-8 and caspase-9, the mRNA expression of Bax, and inhibited the Bcl-2 mRNA expression. Furthermore, the expressions of caspase-3, caspase-8 caspase-9 and Bax were positively correlated with ROS level, but negatively correlated with T-AOC in testis. In summary, T-2 toxin caused spermatogenesis disorder associated with the germ cell apoptosis medicated by oxidative stress, impairing the male reproductive function.

The effect of fluoride as an ongoing topic has attracted much attentions due to the decline in overall human fertility worldwide. However, whether fluorine causes a temporary stimulus or permanent damage to the male reproductive system, as well as the mechanism of fluoride influencing spermatogenesis remained unclear. 48 adult male rats were randomly divided into four groups (twelve each). Control group received the distilled water, while the other three groups were treated with 25, 50, 100 mg/L NaF via drinking water for 8 weeks. Six rats from each group were selected randomly to detect the levels of various indices related to spermatogenesis. The remaining rats were given only distilled water and left for recovery of a period of 2 weeks. Results showed that the levels of serum CK, ALP, CHE, BUN, UA, and Cr, testis morphology and the ultrastructure of sperm acrosome and chromatoid body (CB) were significantly changed by fluoride. Interestingly, the elongated spermatid counts, spermatids elongation ratio, and mRNA expressions of Prm1/2 and MIWI, TDRD1, TDRD 6, TDRD7, PABP, and Hsp72 related to CB decreased markedly in fluoride treatment groups compared to the control. Furthermore, the expression levels of DDX25 and associated regulatory proteins like CRM1, HMG2, H4, TP2, and PGK2 were down-regulated by fluoride. After 2-weeks withdrawal period, out of the 19 altered spermatogenesis indicators, 15 indicators in 100 mg/L group and 3 indicators in 50 mg/L group still exhibited a significant change, while none showed change in 25 mg/L group. These results proved that the reversibility of fluoride toxicity is dose-dependent on the male reproductive system. Meanwhile, fluoride caused unrestored arrest during the haploid period of spermatogenesis, where reduced DDX25 and associated regulatory proteins play a crucial role in this process, which could provide the underlying insights to the toxic mechanism of fluoride induced male reproductive toxicity.

Microplastics are a contaminant of emerging concern which enter the marine environment from a variety of sources. The ingestion and toxic effects of microplastics on marine life, especially for filter feeders, are a cause of concern in view of their ubiquitous nature and their similar size as food sources. To assess the toxic effects of microspheres ingested by brine shrimp larvae, we exposed Artemia parthenogenetica to 10 μm polystyrene microspheres at different concentrations. These concentrations were approximate to the extrapolated marine aquatic environmentally relevant concentrations. The lowest polystyrene concentrations at which ingestion was visualized in A. parthenogenetica were 12 ± 0.57 particles/mL (6.7 ± 0.32 μg/L) and 1.1 ± 0.16 particles/mL (0.61 ± 0.088 μg/L), respectively. There were no significant impacts on the survival, growth or development in A. parthenogenetica occurring over the 14-d exposure across a range of polystyrene nominal concentrations (1–1000 particles/mL or 0.55–550 μg/L). However, abnormal ultrastructures of intestinal epithelial cells were observed upon exposure to polystyrene microspheres, including fewer and disordered microvilli, an increased number of mitochondrion and the appearance of autophagosome. These phenomena could affect nutrition absorption and energy metabolism. Although no major acute or chronic toxicity effects on A. parthenogenetica were observed over 24-h or 14-d exposures, this study provides evidence that the ingestion of polystyrene microplastics at extrapolated environmentally relevant concentrations can be visualized through a microscope to be causing a series of responses in intestinal epithelial cells.

Although, health and environmental hazards of Ni are ironclad; however, that of Nickle oxide nanoparticles (NiO-NPs) are still obscure. Therefore, impact of NiO-NPs exposure (0, 5, 50, 200, 500 and 1000 mg kg⁻¹ soil) on the earthworm (Eisenia fetida) survival (at 28th day), reproduction (at 56th day), histopathology, ultrastructures, antioxidant enzymes and oxidative DNA damage was appraised in full life cycle study. Lower concentrations of NiO-NPs (5, 50 and 200) did not influence the survival, reproduction and growth rate of adult worms significantly. However, reproduction reduced by 40–50% with 500 and 1000 mg kg⁻¹ exposure, which also induced oxidative stress leading to DNA damage in earthworms. Ultrastructural observation and histology of earthworms exposed to higher NiO-NPs concentrations revealed abnormalities in epithelium layer, microvilli and mitochondria with underlying pathologies of epidermis and muscles, as well as adverse effects on the gut barrier. To the best of our knowledge, this is the first study unveiling the adverse effects of NiO-NPs on a soil invertebrate (Eisenia fetida). Our findings clue towards looking extensively into the risks of NiO-NPs on soil organisms bearing agricultural and environmental significance.

Due to increased use of agrochemicals and growing concerns about ecotoxicology, the development of new insecticides, moving away from those with neurotoxic and broad spectrum effects towards insecticides that are safer for the environment and nontarget beneficial species, has been a research priority. Novaluron stands out among these newer insecticides, is an insect growth regulator that is used for the control of insect pests in crops grown close to mulberry plantations. Mulberry serves as food for the silkworm Bombyx mori, which is a nontarget insect of great economic importance to silk production. We investigated the lethal and sublethal effects of Novaluron on the development of B. mori. Larvae were segregated into experimental groups: the control groups (CGs) and the treatment groups (TGs), which were treated with the Novaluron concentration of 0.15 mL/L. Following exposure, we analyzed: larval mortality, changes in the insect life cicle and cytotoxic effects on the midgut cells. This is the first report about the Novaluron’s effects on B.mori. We detected rupture in the integument, complete cessation of feeding, late development, incomplete ecdysis and production of defective cocoons. After 240 h of exposure, there was 100% mortality in TG larvae exposed in the 3rd instar and 20% mortality from larvae exposed in the 5th instar. Cytotoxic effects was observed, such as dilation of cells, emission of cytoplasmic protrusions, extreme rarefaction of the cytoplasm and nuclei, dilation of the endoplasmic reticulum in addition to changes in mitochondria, the presence of large digestive vacuoles and intercellular spaces and the presence of active caspase. Novaluron exposure impairs the midgut and may affect the physiological functions of this organ. Novaluron additionally compromises several phases of insect development, indicating the importance of toxicology studies that utilize different life stages of nontarget species to evaluate the safe use of insecticides.

Microcystins (MCs) widely distributed in freshwaters have posed a significant risk to human health. Previous studies have demonstrated that exposure to MC-LR impairs pancreatic islet function, however, the underlying mechanisms still remain unclear. In the present study, we explored the role of endoplasmic reticulum (ER) impairment in β-cell dysfunction caused by MC-LR. The result showed that MC-LR modified ER morphology evidenced by increased ER amount and size at low doses (15, 30 or 60 μM) and vacuolar and dilated ER ultrastructure at high doses (100 or 200 μM). Also, insulin content showed increased at 15 or 30 μM but declined at 60, 100, or 200 μM, which was highly accordant with ER morphological alteration. Transcriptomic analysis identified a number of factors and several pathways associated with ER protein processing, ER stress, apoptosis, and diabetes mellitus in the cells treated with MC-LR compared with non-treated cells. Furthermore, MC-LR-induced ER stress significantly promoted the expression of PERK/eIF2α and their downstream targets (ATF4, CHOP, and Gadd34), which indicates that PERK-eIF2α-ATF4 pathway is involved in MC-LR-induced insulin deficiency. These results suggest that ER impairment is an important contributor to MC-LR-caused β-cell failure and provide a new insight into the association between MCs contamination and the occurrence of human diseases.