Impact of chromium and boron compounds on the reproductive function in ratsMarat, Iztleuov; Arstan, Mamyrbayev; Galymzhan, Yeleuov; Timur, Jarkenov; Yerbolat, Iztleuov; Almasbek, Yeleuov
doi: 10.1177/0748233718759162pmid: 29591889
The purpose of this research is to study the process of mutagenesis and the reproductive function in male rats under separate and combined exposure to chromium and boron compounds. The experiment was conducted on two groups of animals. The first group was used to assess the ability of potassium dichromate and boric acid to induce mutation in germ and somatic cells under isolated and combined administration with the use of the dominant lethal mutations test and the micronuclei test in the polychromatophilic erythrocytes of the bone marrow. The second group was used to test the combined and separate effect of the compounds under consideration on the reproductive function of male rats during the spermatogenesis cycle. When used in specific doses, boron compounds are a promising means of preventing and correcting chromium-induced effects in chromium production facility workers and people who live in ecologically adverse regions.
Investigation of the genotoxic and cytotoxic effects of widely used neonicotinoid insecticides in HepG2 and SH-SY5Y cellsŞenyildiz, Mine; Kilinc, Adem; Ozden, Sibel
doi: 10.1177/0748233718762609pmid: 29591886
Neonicotinoids are a relatively new type of insecticide to control a variety of pests. Although they are generally considered to be safe, they can lead to harmful effects on human and environmental health. We aimed to investigate possible effects of common neonicotinoid insecticides (acetamiprid, clothianidin, imidacloprid, thiacloprid, and thiamethoxam) on cytotoxicity and DNA damage in human neuroblastoma (SH-SY5Y) and human hepatocellular carcinoma (HepG2) cells. Our results indicated that 50% of inhibitory concentration values of neonicotinoids are in the range of 0.96 to >4 mM in SH-SY5Y cells and 0.53 to >4 mM in HepG2 cells by the methyl tetrazolium and neutral red uptake tests after 24 and 48 h exposure. We observed significant DNA damage at 500 µM of five neonicotinoids in SHSY-5Y cells, while only imidacloprid, thiametoxam, and thiacloprid showed some alterations in HepG2 cells after 24 h exposure using the alkaline comet assay. In conclusion, neonicotinoid insecticides may induce cytotoxicity and DNA damage in cell cultures; therefore, further studies are needed to better understand the toxicity of neonicotinoids.
Pathology of cigarettes on the reproductive system and ameliorative effects of alpha lipoic acid: A rat model studyAsci, Halil; Erol, Onur; Ellidag, Hamit Yasar; Tola, Esra Nur; Savran, Mehtap; Ozmen, Ozlem
doi: 10.1177/0748233718755160pmid: 29591887
Cigarette smoking (CS) has some detrimental effects that occur via oxidative stress (OS). The aim of this work was to demonstrate the pathological and immunohistochemical effects of CS and the protective effects of a strong antioxidant alpha lipoic acid (ALA) on CS-induced genital system changes in a rat model. Twenty-eight female rats were randomly allocated to three groups as control, CS-exposed, and CS-exposed and ALA-treated. Reproductive tract organs were collected for biochemical and pathological examinations. In the CS group, OS markers increased in the tissues of both the ovary and fallopian tubes. Decreased follicle numbers in the ovary, marked cilial loss in the fallopian tubes, and pathologic changes in the uterus were observed in the CS group. Positive calcitonin gene–related peptide (CGRP), caspase 3α, hypoxia-inducible factor 1α (HIF-1α), tumor necrosis factor-α (TNF-α) immunoreactions were observed in uterine tissues and HIF-1α immunoreactions in tubal and uterine epithelial cells of the CS group. ALA reversed all these findings effectively. CS has negative effects on the female reproductive system via HIF-1α in tuba uterina and HIF-1α, HIF-2α, TNF-α, caspase 3, and CGRP in the uterus, and ALA could protect against the negative effects of CS on the female reproductive system.
Suppressive effects of neonatal bisphenol A on the neuroendocrine systemAhmed, RG; Walaa, GH; Asmaa, FS
doi: 10.1177/0748233718757082pmid: 29656705
The aim of this study was to assess the effects of neonatal bisphenol A (BPA) administration on neuroendocrine features (the thyroid–brain axis). BPA (20 or 40 µg/kg) was orally administered to juvenile male albino rats (Rattus norvegicus) from postnatal days (PNDs) 15 to 30. Both doses resulted in lower serum thyroxine (T4), triiodothyronine (T3), and growth hormone levels and higher thyrotropin level than the control levels at PND 30. In the neonatal cerebellum and cerebrum, vacuolation, pyknosis, edema, degenerative changes, and reductions in the size and number of the cells were observed in both treated groups. Alternatively, elevations in oxidative markers (lipid peroxidation, nitric oxide, and hydrogen peroxide [H2O2]) at both dose levels were recorded at PND 30, along with decreased activities of antioxidant markers (ascorbic acid, total thiol [t-SH], glutathione, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, and catalase) with respect to control levels. Thus, the BPA-induced hypothyroid state may disturb the neonatal thyroid–brain axis via production of free radicals, and this could damage the plasma membrane and cellular components, delaying cerebrum and cerebellum development.
Nano-CuO impairs spatial cognition associated with inhibiting hippocampal long-term potentiation via affecting glutamatergic neurotransmission in ratsLi, Xiaoliang; Sun, Wei; An, Lei
doi: 10.1177/0748233718758233pmid: 29665767
Manufactured metal nanoparticles and their applications are continuously expanding because of their unique characteristics while their increasing use may predispose to potential health problems. Several studies have reported the adverse effects of copper oxide nanoparticles (nano-CuO) relative to ecotoxicity and cell toxicity, whereas little is known about the neurotoxicity of nano-CuO. The present study aimed to examine its effects on spatial cognition, hippocampal function, and the possible mechanisms. Male Wistar rats were used to establish an animal model, and nano-CuO was administered at a dose of 0.5 mg/kg/day for 2 weeks. The Morris water maze (MWM) test was employed to evaluate learning and memory. The long-term potentiation (LTP) from Schaffer collaterals to the hippocampal CA1 region, and the effects of nano-CuO on synases were recorded in the hippocampal CA1 neurons of rats. MWM test showed that learning and memory abilities were impaired significantly by nano-CuO (p < 0.05). The LTP test demonstrated that the field excitatory postsynaptic potential (fEPSP) slopes were significantly lower in nano-CuO-treated groups compared with the control group (p < 0.01). Furthermore, the data of whole-cell patch-clamp experiments showed that nano-CuO markedly depressed the frequencies of both spontaneous excitatory postsynaptic currents (sEPSCs) and miniature EPSCs (mEPSCs), indicating an effect of nano-CuO on inhibiting the release frequency of glutamate presynapticly (p < 0.01). Meanwhile, the amplitudes of both sEPSC and mEPSC were significantly reduced in nano-CuO-treated animals, which suggested that the effect of nano-CuO modulates postsynaptic receptor kinetics (p < 0.01). Paired pulse facilitation (PPF) (p < 0.05) and the expression of NR2A, but not NR2B, of N-methyl-d-aspartate (NMDA) subunits (p < 0.05), were decreased significantly. In conclusion, nano-CuO impaired glutamate transmission presynapticly and postsynapticly, which may contribute importantly to diminished LTP and other induced cognitive deficits.
Sublethal chronic effects of oral dietary exposure to deltamethrin in Swiss albino miceTewari, Anita; Banga, HS; Gill, JPS
doi: 10.1177/0748233718758913pmid: 29665769
The hazards of dietary exposure to environmentally relevant levels of deltamethrin are poorly understood though studies enunciate the acute toxicity hazards. In this study, prolonged exposure to low levels of deltamethrin in mice was investigated. The mice were exposed daily via gavage method for 60 days. Four doses (0.1, 0.05, 0.01, and 0.005 mg/kg bwt/d) were selected, which are equal to or less than the maximum residue limits for deltamethrin permitted in animal food/feed. Liver, kidney, lungs, spleen, and testes were collected on day 61 for histology, residue, and biochemical analysis (aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALKP), total bilirubin (TBIL), total proteins (TPs), cholesterol (CHOL), urea, and creatinine). No significant changes were observed in body weight gain in all treatment groups (p > 0.05). The gas chromatography analysis indicated that none of the tissue samples contained deltamethrin residues above the limits of quantification. The significant differences in biochemical profile (AST, ALT, TBIL, and creatinine) reported in animals exposed to 0.1 and 0.05 mg/kg bwt/d deltamethrin (p < 0.05) suggest respective tissue injury and lipid peroxidation; however, few significant changes in urea and CHOL were also reported in doses 0.01 and 0.005 mg/kg bwt. No significant differences in TP and ALKP were observed (p > 0.05). The target organs for deltamethrin toxicity showed prominent histopathological changes in concentrations of 0.1 and 0.05 mg/kg bwt. Other two doses showed no or sporadic changes. Our findings suggest that chronic exposure to environmentally relevant levels of deltamethrin can have detrimental effects on vital organs in the circumstances allowing daily exposure, in congruence with available literature.
Support to triage and public risk perception considering long-term response to a Cs-137 radiological dispersive device scenarioAndrade, Cristiane PS; Souza, Cláudio J; Camerini, Eduardo SN; Alves, Isabela S; Vital, Hélio C; Healy, Matthew JF; Ramos De Andrade, Edson
doi: 10.1177/0748233718762920pmid: 29665768
A radiological dispersive device (RDD) spreads radioactive material, complicates the treatment of physical injuries, raises cancer risk, and induces disproportionate fear. Simulating such an event enables more effective and efficient utilization of the triage and treatment resources of staff, facilities, and space. Fast simulation can give detail on events in progress or future events. The resources for triage and treatment of contaminated trauma victims can differ for pure exposure individuals, while discouraging the “worried well” from presenting in the crisis phase by media announcement would relieve pressure on hospital facilities. The proposed methodology integrates capabilities from different platforms in a convergent way composed of three phases: (a) scenario simulation, (b) data generation, and (c) risk assessment for triage focused on follow-up epidemiological assessment. Simulations typically indicate that most of the affected population does not require immediate medical assistance. Medical triage for the few severely injured and the radiological triage to diminish the contamination with radioactivity will always be the priority. For this study, however, higher priorities should be given to individuals from radiological “warm” and “hot” zones as required by risk criteria. The proposed methodology could thus help to (a) filter and reduce the number of individuals to be attended, (b) optimize the prioritization of medical care, (c) reduce or prepare for future costs, (d) effectively locate the operational triage site to avoid possible contamination on the main facility, and (e) provide the scientific data needed to develop an adequate approach to risk and its proper communication.