Pyrethroids, which are synthetic derivatives of naturally occurring pyrethrins, are world-class insecticides used for both agricultural and household appliances. Since their invention, the contributions to the increasing global demand for food and public health are unquestionable. Nevertheless, the indiscriminate use of these compounds resulted in the last decades in substantial damaging effects on health and the environment. In this chapter, elements from literature related to the mitochondrial aspects involved in pyrethroids-induced toxicity are presented. It is shown that in addition to the classical mechanism of toxicity involving voltage-gated sodium channels, these compounds can act in a myriad of cellular and molecular targets that ultimately converge to the disruption of mitochondrial function and neurotoxicity.
Background Early-life stress, such as maternal deprivation (MD), is a stressor that can lead to cognitive deficits in adulthood. Among the neurochemical mechanisms involved in MD-induced pathophysiology are alterations in the dopaminergic and noradrenergic systems. We recently demonstrated that pharmacological stimulation of dopaminergic neurons in the ventral tegmental area (VTA) improves novel object recognition (NOR) memory in rats subjected to MD. Furthermore, projections from the locus coeruleus (LC) to the dorsal hippocampus (DH) are important for memory consolidation. Methods From postnatal day (PND) 1–PND10, male and female rats were either subjected to MD or left undisturbed. In adulthood, the animals underwent stereotaxic surgery for bilateral cannulation of the DH and LC. Following recovery and habituation, the animals were trained in the NOR task and immediately received vehicle or timolol in the DH, and either vehicle or NMDA in the LC. NOR memory was assessed at 24 h, as well as 7 and 14 d after training, to evaluate memory consolidation and persistence, respectively. Results MD impaired NOR memory in male rats, but not in females. Pharmacological stimulation of the LC with NMDA promoted NOR memory persistence in both non-MD and MD males and females. In males, LC stimulation also reversed the MD-associated memory impairment. These effects were maintained despite hippocampal β-adrenergic receptor blockade with timolol. Conclusion These findings suggest that LC-related pathways contribute to the processing of NOR memory persistence following early-life stress in a sex-dependent manner. This effect appears to be independent of hippocampal β-adrenergic signaling.
Plant species richness can provide a range of benefits to the soil, since mixtures of species with contrasting functional traits enhance soil organic carbon (SOC) stocks. However, there is still limited information on the impact of increased plant species richness on tropical forage systems. This study evaluated whether increasing plant species affects soil quality attributes and forage yield in a tropical ecosystem. The experiment consisted of five treatments: 1) very low—single grass (Urochloa brizantha); 2) low – grass intercropped with cowpea; 3) medium – MIX with grass intercropped with cowpea and buckwheat; 4) high – MIX with grass intercropped with cowpea, buckwheat and forage radish; and 5) very high – MIX with grass intercropped with cowpea, buckwheat, forage turnip and sunflower. Increasing species richness altered root mass without reducing forage yield. Compared with the very low richness treatment, the very high richness significantly increased microbial biomass carbon (C) (130
Insect-derived proteins have emerged as promising sustainable alternatives to conventional edible proteins, owing to their low greenhouse gas emissions, high feed conversion efficiency, reduced water requirements, and cost-effectiveness. This study investigated the extraction of proteins from the larval biomass of two fly species through alkaline solubilization followed by isoelectric precipitation. The resulting protein isolates were characterized in terms of protein content and extraction yield, infrared spectroscopy, differential scanning calorimetry, amino acid composition, in vitro digestibility, and antioxidant capacity. The highest protein content was obtained from Musca domestica (59.7
In the present study, the effect of 6-((4-fluorophenyl) selanyl)-9H-purine (FSP) was tested against memory impairment and sensitivity to nociception induced by intracerebroventricular injection of amyloid-beta peptide (Aβ) (25–35 fragment), 3 nmol/3 μl/per site in mice. Memory impairment was determined by the object recognition task (ORT) and nociception by the Von-Frey test (VFT). Aβ caused neuroinflammation with upregulation of glial fibrillary acidic protein (GFAP) (in hippocampus), nuclear factor-κB (NF-κB), and the proinflammatory cytokines interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) in cerebral cortex and hippocampus. Additionally, Aβ increased oxidant levels and lipid peroxidation in cerebral cortex and hippocampus, but decreased heme oxygenase-1 (HO-1) and peroxiredoxin-1 (Prdx1) expression in the hippocampus. Anti-neuroinflammatory effects of FSP were demonstrated by a decrease in the expression of GFAP and NF-κB in the hippocampus, as well as a decrease in proinflammatory cytokines in both the hippocampus and cerebral cortex FSP protected against oxidative stress by decreasing oxidant levels and lipid peroxidation and by increasing HO-1 and Prdx1 expressions in the hippocampus of mice. Moreover, FSP prevented the activation of nuclear factor erythroid 2-related factor 2 (Nrf-2) in the hippocampus of mice induced by Aβ. In conclusion, treatment with FSP attenuated memory impairment, nociception sensitivity by decreasing oxidative stress, and neuroinflammation in a mouse model of Alzheimer’s disease.
