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Layered double hydroxide (LDH) nanomaterials have recently become immense research area as it is used widely in industries. So, it's chance of their release into natural environment and risk assessment to nontarget aquatic invertebrate increasing. So, the present study aimed to synthesize and confirm the crystalline formation of Co-Cd-Fe LDHs and Co-Cd-Fe/PbI 2 (LDH) and then to investigate the toxic impact of the two LDH on the adult freshwater snails (Biomphalaia alexandrina). Results showed that Co-Cd-Fe/PbI 2 LDH has more toxic effect to adult Biomphalaria than Co-Cd-Fe LDHs (LC 50 was 56.4 and 147.7 mg/L, 72 h of exposure, respectively). The effect of LC 25 (117.1 mg/L) of Co-Cd-Fe LDHs exposure on the embryo showed suppression of embryonic development and induced embryo malformation. Also, it showed alterations in the tegmental architectures of the mantle-foot region of B. alexandrina snails as declared in scanning electron micrograph. Also, exposure to this sublethal concentration caused abnormalities in hemocyte shapes and upregulated IL-2 level in soft tissue. In addition, it decreased levels of nonenzymatic reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), caspase-3 activity, and total protein content in significant manner. Glutathione S-transferase (GST) activity was not affected by LDH exposure. It caused histopathological damages in both glands of snails and also caused a genotoxic effect in their cells. The results from the present study indicated that LDH has risk assessment on aquatic B. alexandrina snails and that it can be used as a biological indicator of water pollution with LDH., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

The pyrethroid imiprothrin is widely used worldwide for control of insects in the agriculture and public health sectors. No sufficient information is however available concerning detoxification gene expression, i.e., cytochrome P450 1A2 (CYP1A2) and metallothionein 1a gene, oxidative stress, lipid peroxidation, DNA damage, cytotoxicity, genotoxicity, and organ injury induced by imiprothrin in mammals. This study is designed to explain the mechanism of imiprothrin induced detoxification gene expression, DNA damage, cytotoxicity, genotoxicity, and organ toxicity in male rats. The benchmark dose (BMD) was calculated to find the best sensitive markers to imiprothrin toxicity. Imiprothrin was injected intraperitoneally (i.p.) into male rats once a day for 5 days with doses of 19, 38, and 75 mg/kg body weight (b.wt.). Imiprothrin caused a significant increase in lipid peroxidation and changes in oxidative stress biomarkers in treated rats. Significant dose-dependent changes in the liver and kidney biomarkers were observed. Histopathological alterations were seen in the liver and kidney tissue of male rats. Imiprothrin also significantly increased chromosomal aberrations (CA) and micronuclei in bone-marrow cells, and induced lipid peroxidation, oxidative stress, cytotoxicity, and liver and kidney dysfunction, and damage. Imiprothrin induced DNA damage and over detoxification gene expression of CYP1A2 and metallothionein 1a gene in hepatocytes of male rats. Imiprothrin thus shows clastogenic and genotoxic potential. The mechanism for hepatorenal toxicity and injury, genotoxicity/cytotoxicity of imiprothrin might be due to enhanced lipid peroxidation, and oxidative stress associated with overproduction of free radicals, especially reactive oxygen species, and an imbalance in redox status. From the BMD models, aspartate aminotransferase (AST), total protein, uric acid, superoxide dismutase (SOD), and micronuclei (MPEs) were very sensitive markers to imiprothrin toxicity.

Being the largest agriculture country in the Arab world, Egypt was one of the major consumer of organochlorine pesticides (OCPs) in this area, continued to have a heavy burden of OCPs in the environment. There is growing concern that OCPs could pass from the maternal circulation through the placenta to the fetal circulation and pose several health risks to their fetuses. The current study was intended to identify OCPs residue exposure in healthy pregnant women and to justify the potential impacts of these residues on their fetuses. In this study, the prevalence of 18 OCPs was estimated in 81 maternal and cord blood samples, using Agilent 7890, gas chromatograph equipped with micro-electron capture detector (GC-μECD). Our data signposted that the heptachlor epoxide has the highest detection rate among all residues in both maternal (32%) and cord blood serum (27.16%). DDTs were still quantifiable, but with the lowest quantifiable percentage. More than 85% of mothers' serum with detectable residues transfer OCPs residue to their fetuses in a statistically significant manner (x = 42.9, p value < 0.001). The present findings showed no significant growth retardation, or preterm delivery induced by in utero exposure to the most abundant residues. There is growing evidence that exposure to OCPs residue has profound impact on sex ratio. Methoxychlor, in this study be deemed as testosterone triggers which yields high boys ratio (x = 4.37, p < 0.05). In conclusion, Egypt continued to have a heavy burden of OCPs residues, and fetuses and infants are especially the most vulnerable groups to their adverse health effects. Exposure to OCPs may disrupt the maternal hormones, which regulate the offspring gender, but these results need to be validated in larger sample sizes.

The present study is the first report for studying the toxic effects of butralin herbicide on COX2, BAX, and Bcl2 gene expression, oxidative stress, and liver damage in female rats. Female rats were received butralin in drinking water for 28 days at concentration 4.16, 312, and 3120 mg/L that corresponded to the acceptable daily intake (ADI), no observed adverse effect level (NOAEL), and 10 NOAEL, respectively. Butralin decreased body weights and increased relative liver weight of female rats exposed to high dose. It caused significant elevation in liver function enzymes, lipid peroxidation, and reactive oxygen species (ROS). Antioxidant enzymes were decreased in liver tissue by increasing the dose. Butralin induced over-expression in the apoptotic related genes including COX2, BAX, and Bcl2 and pathological alteration in the liver of female rats especially at a high dose. It can be concluded that butralin induced oxidative damage and liver injure. The mechanism of damage could be due to generate reactive oxygen species, and increase lipid peroxidation that causes over-expression in the apoptotic related genes including COX2, BAX, and Bcl2. From the Benchmark dose (BMD) approach, there is dose-dependent manner in body weight, AST, ALT, and ALP, and ALT is a very sensitive parameter.

Green and nanoacaricides including essential oil (EO) nanoemulsions are important compounds to provide new, active, safe acaricides and lead to improvement of avoiding the risk of synthetic acaricides. This study was carried out for the first time on eriophyid mites to develop nanoemulsion of garlic essential oil by ultrasonic emulsification and evaluate its acaricidal activity against the two eriophyid olive mites Aceria oleae Nalepa and Tegolophus hassani (Keifer). Acute toxicity of nanoemulsion was also studied on male rats. Garlic EO was analyzed by gas chromatography-mass spectrometry (GC-MS), and the major compounds were diallyl sulfide (8.6%), diallyl disulfide (28.36%), dimethyl tetrasulfide (15.26%), trisulfide,di-2-propenyl (10.41%), and tetrasulfide,di-2-propenyl (9.67%). Garlic oil nanoemulsion with droplet size 93.4 nm was formulated by ultrasonic emulsification for 35 min. Emulsification time and oil and surfactant ratio correlated to the emulsion droplet size and stability. The formulated nanoemulsion showed high acaricidal activity against injurious eriophyid mites with LC 50 298.225 and 309.634 μg/ml, respectively. No signs of nanoemulsion toxicity were noted in treating rats; thus, it may be considered non-toxic to mammals. Stability of garlic oil nanoemulsion, high acaricidal activity, and the absence of organic toxic solvents make the formulation that may be a possible acaricidal product. Results suggest the possibility of developing suitable natural nanoacaricide from garlic oil.

Information about the adverse effects of lactation transfer of abamectin (ABA) is important for human health, especially in the third-world countries where breastfeeding is the only source of nutrition for infants. So, the present study was undertaken to evaluate the adverse effects of breastfeeding exposure to ABA on oxidative damage and liver and kidney dysfunction in suckling rats. Dams were orally administered ABA at a doses 22.10, 11.05, and 2.21 mg a.i./kg b.wt from postnatal day 1 (PND1) until day 20 (PND20). The signs of toxicity and high mortality were recorded in suckling male (67.5%) and female (55.0%) pups whose mother exposed to the ABA at dose 22.1 mg a.i./kg b.wt. ABA induced significantly decrease in body weights of mothers and their male and female pups and significant increase in relative liver weights. It caused oxidative stress in the liver and kidney of mothers and their pups by increasing the level of malondialdehyde (MDA) and decreased activities of superoxide dismutase (SOD) and glutathione-transferase (GST). ABA altered the level of serum liver and kidney dysfunction biomarkers either in the mothers or their male and female pups in a dose-dependent manner. It caused histopathological alterations in the liver and kidney tissues. It can be decided that ABA was accumulated in mother's milk, transferred through breast feeding, and induced mortality in their suckling pups. It caused oxidative stress, lipid peroxidation, and biochemical and histopathological alterations in the liver and kidney of mothers and their suckling pups. The results in the present study add some information about the adverse effect of lactation transfer of ABA, which is important for human health in the third-world countries where breastfeeding may be the only source of nutrition for infants in the first and most critical weeks of life.