e. detoxification of certain insecticides, but activation of others pro-insecticides). The goal of this review is to critically summarise the current knowledge and the gaps of the CYP-based metabolic insecticide resistance in Anopheles and Aedes mosquito vectors. The progress and limitations of the protein and the reverse/forward genetic approaches, the understanding and importance of molecular and physiological aspects, as well as the current and future exploitation routes of CYP research are discussed.To evaluate whether the development of β-cypermethrin resistance in Blattella germanica (L.) (Blattaria Blattellidae) affects the fecundity fitness of this insect and to determine the underlying mechanism, we compared fecundity differences between β-cypermethrin-resistant (R) and sensitive (S) strains of B. germanica, observed the physiological structural changes of ovaries from an visual perspective, and analyzed differences in the ovarian proteome using proteomic methods. The results showed that, compared with the S strain of B. germanica, the R strain of B. germanica had a significantly higher ootheca shedding rate, a significantly lower number of hatched and surviving nymphs, a significantly higher female proportion in the population and defective ovarian development. Ovarian proteomic analysis showed a total of 64 differentially expressed proteins in the R strain, including 18 upregulated proteins and 46 downregulated proteins. Twenty-four significantly differentially expressed proteins were further studied, and 14 were successfully identified, which were mainly classified into the following categories immunity-related proteins, development-related proteins, structural proteins, energy metabolism-related proteins and proteins with unknown functions. The differential expression of these proteins reflects the overall changes in cell structure and metabolism associated with β-cypermethrin resistance and explains the possible molecular mechanism of fecundity fitness disadvantages. In summary, β-cypermethrin resistance can cause fecundity fitness disadvantages in B. germanica. The metabolic deviations needed to overcome the adverse effects of insecticides may result in an energy exchange that affects energy allocation and, ultimately, the basic needs of the insect. The fitness cost due to insecticide resistance is critical to the delay of the evolution of resistance.For the last decade, scientists have reported a loss of honeybee colonies. Multiple factors like parasites, pathogens and pesticides are dealt as possible drivers of honeybee losses. In particular, insecticides are considered as a major factor of pollinator poisoning. We applied sublethal concentrations of four insecticidal substances to honeybee larval food and analyzed the effects on transcriptome. The aim was to identify candidate genes indicating early negative impacts after application of insecticidal substances. Honeybee larvae were kept in-vitro under hive conditions (34-35 °C) and fed with dimethoate, fenoxycarb, chlorantraniliprole and flupyradifurone in sublethal concentrations between day 3-6 after grafting. Larvae at day 4, 6 and 8 were sampled and their transcriptome analyzed. By use of a RT-qPCR array differences in gene expression of selected gene families (immune system, development detoxification) were measured. Targets mainly involved in development, energy metabolism and the immune system were significantly affected by the insecticidal substances tested, selectively inducing genes of the detoxification system, immune response and nutritional stress.New insecticides are urgently needed for the control of arthropod vectors of public health diseases. As resistance to many insecticides used for the control of public health pests is ubiquitous, all available chemistries should be evaluated for their potential to effectively control both insecticide-susceptible and insecticide-resistant strains of mosquitoes.  https://www.selleckchem.com/products/cp2-so4.html  This study aimed to evaluate p-p'-difluoro-diphenyl-trichloroethane (DFDT) as a mosquito control technology and relate its activity to that of DDT. We found that topical DFDT was significantly less toxic than DDT to both pyrethroid-susceptible and pyrethroid-resistant strains of Anopheles gambiae and Aedes aegypti. Direct nervous system recording from Drosophila melanogaster CNS demonstrated that DFDT is approximately 10-times less potent than DDT at blocking nerve firing, which may explain its relatively lower toxicity. DFDT was shown to be at least 4500 times more vapor-active than DDT, with an LC50 in a vapor toxicity screening assay of 2.2 μg/cm2. Resistance to DFDT was assessed in two mosquito strains that possess target-site mutations in the voltage-gated sodium channel and upregulated metabolic activity. Resistance ratios for Akdr (An. gambiae) and Puerto Rico (Ae. aegypti) strains were 9.2 and 12.2, respectively. Overall, this study demonstrates that DFDT is unlikely to be a viable public health vector control insecticide.TEB belongs to the family of triazole fungicides and it is used to protect agricultural crop plants from fungal pathogens. The information regarding its cardiotoxic effects through different pathways particularly by perturbing the oxidative balance and causing damage to the myocardium is still limited. In the present study, oxidative and histopathologic damages caused by TEB in the cardiac tissue of male adult rats, were evaluated. Rats were exposed orally to TEB at 0.9, 9, 27 and 45 mg/kg b.w. for 28 days. Results showed that following TEB treatment malondialdehyde (MDA), protein carbonyl (PC), advanced oxidation protein product (AOPP), antioxidant enzyme activities (GPx and GR) and GSSG levels increased, while GSH levels and thus the GSH/GSSG ratio decreased. Superoxide dismutase (SOD) and catalase (CAT) initially increased at the doses of 0.9, 9 and 27 mg/kg b.w. and then decreased at the dose of 45 mg/kg b.w. Moreover, western blot analysis showed that TEB increased SOD1, CAT and HSP70 protein levels after 24 h. Furthermore, TEB induced various histological changes in the myocardium, including leucocytic infiltration, hemorrhage congestion of cardiac blood vessels and cytoplasmic vacuolization. Therefore, our investigation revealed, that TEB exhibits cardiotoxic effects by changing oxidative balance and damaging the cardiac tissue.