RESUMEN
Abamectin (AB) is widely used in agriculture and has been employed as an insecticide, nematicide, and livestock pest control agent. However, it may also pose a serious threat to mammals. The primary purpose of this research was to compare the sex variations between male and female rats during exposure and to assess the risk of toxicity of abamectin, which are still largely unknown. The twenty albino rats were divided randomly into four groups (n = 5): 1) the male control group; 2) the male treatment group treated with AB (1 mg/kg B.W.); 3) the female control group; and 4) the female treatment group treated with AB (1 mg/kg B.W.). AB administration caused a drop in body weight in females more than males with showing oxidative stress in both sexes of animals, as characterized by an increase in MDA content and a decrease in glutathione (GSH) content and superoxide dismutase (SOD) activity. Reported sex-specific effects suggested that females are more susceptible from males in brain tissues for alteration of antioxidant markers while females' liver and kidney tissues showed more level of lipid peroxidation than males. In addition, mitochondrial dysfunction was associated with a significant decrease in NADH dehydrogenase (Complex I) and a significant decrease in mitochondrial ATPase, which led to apoptosis and histopathological alterations in the targeted tissues, indicating that females are higher sensitive than males to these biological events. In brief, the results of this study led to female rats are generally more sensitive than male rats to neurobehavioral and hepatic complications associated with abamectin treatment. Further evaluation should be performed to determine the adverse outcome pathways involved and to determine the effects of sex on improving the risk assessment of abamectin in both sexes.
Asunto(s)
Apoptosis , Ivermectina , Ivermectina/análogos & derivados , Mitocondrias , Estrés Oxidativo , Animales , Ivermectina/toxicidad , Femenino , Masculino , Estrés Oxidativo/efectos de los fármacos , Apoptosis/efectos de los fármacos , Ratas , Mitocondrias/efectos de los fármacos , Mitocondrias/metabolismo , Glutatión/metabolismo , Superóxido Dismutasa/metabolismo , Hígado/efectos de los fármacos , Hígado/metabolismo , Hígado/patología , Peroxidación de Lípido/efectos de los fármacos , Riñón/efectos de los fármacos , Riñón/metabolismo , Riñón/patología , Malondialdehído/metabolismo , Insecticidas/toxicidadRESUMEN
This investigation was directed to examine the influence of copper oxide nanoparticles (CuO-NPs) on the hatchability traits, and chick quality of newly hatched broiler chicks. A total of 480 eggs were randomly divided into four treatment groups, each consisting of three duplicates. As a negative control (NC), the first group was not injected; the second group was injected with saline and served as a positive control (PC), the third and fourth groups were injected with 30 and 60 ppm of (CuO-NPs)/egg. Eggs were injected into the amniotic fluid on the eighteenth day of the incubation period. Results showed that the hatchability, chick yield %, yolk free-body mass (YFBM), chick length, shank length (SL), and relative weight of the heart, gizzard and intestine of day-old broiler chicks were all unaffected by the in ovo injection of CuO-NPs. The Pasgar Score was slightly improved compared to the NC and PC groups. Also, the in ovo administration of CuO-NPs (60 ppm/egg) significantly increased the intestine length. Both levels of CuO-NPs significantly increased the concentration of Cu ions in the hepatic tissue. Additionally, different levels of tissue damage were seen in the liver of the birds that were given low or high dosages of CuO-NPs. Conclusively, the in ovo injection of CuO-NPs has a good result on the appearance of the chicks (Pasgar score). However, negative effect of CuO-NPs on liver tissue may raise concerns about the potential risks of applying CuO-NPs in ovo administration.
RESUMEN
BACKGROUND: With the recent growth in the applications of silver nanoparticles (Ag-NPs), worries about their harmful effects are increasing. Selenium plays a vital role in the antioxidant defense system as well as free radical scavenging activity. OBJECTIVES: This study aims to inspect the neuroprotective effect of selenium-loaded chitosan nanoparticles (CS-SeNPs) against the adverse impact of Ag-NPs on brain tissue in adult rats. DESIGN: Rats were divided into four groups: group I (control) was administered distilled water (0.5 mL/kg), group II was administered Ag-NPs (100 mg/kg), group III was administered Ag-NPs (100 mg/kg) and CS- SeNPs (0.5 mg/kg) and group IV received only CS- SeNPs (0.5 mg/kg) daily by oral gavage. After 60 days, rats were subjected to behavioral assessment and then euthanized. Brain tissues were obtained for estimation of total antioxidant capacity (TAC), malondialdehyde (MDA), 8-hydroxy-2-deoxy Guanosine (8-OHdG), and Nuclear Factor Erythroid 2 Like Protein 2 (Nrf2). Also, histological examination of the brain and immunohistochemical detection of glial fibrillary acidic protein (GFAP) were investigated RESULTS: exposure to Ag-NPs induced marked neurotoxicity in the brain tissue of rats that was manifested by decreased levels of TAC and Nrf2 with increased levels of MDA and 8-OHdG. Also, various pathological lesions with an increase in the number of GFAP immunoreactive cells were detected. While brain tissue of rats received Ag-NPs plus CS-SeNPs group (III) revealed significantly fewer pathological changes. CONCLUSION: Co-administration of CS-SeNPs significantly ameliorates most of the Ag-NPs-induced brain damage.
Asunto(s)
Quitosano , Nanopartículas del Metal , Nanopartículas , Fármacos Neuroprotectores , Selenio , Ratas , Animales , Selenio/farmacología , Antioxidantes/farmacología , Antioxidantes/metabolismo , Fármacos Neuroprotectores/farmacología , Quitosano/farmacología , Plata/toxicidad , Nanopartículas del Metal/toxicidad , Factor 2 Relacionado con NF-E2/metabolismo , Estrés OxidativoRESUMEN
With recent progress in the manufacture and applications of nickel oxide nanoparticles (NiO NPs), concerns about their adverse effects are increasing. Hesperidin (HSP) is a citrus flavonoid that has a potent anti-inflammatory, antioxidant and free radical scavenging activities. This study aims to investigate the protective effect of HSP against testicular and spermatological damages induced by NiO NPs in male rats. Forty rats were randomly and equally divided into four groups: control, NiO NPs, HSP and NiO NPs + HSP. NiO NPs (100 mg/kg) and/or HSP (100 mg/kg) were given daily by gavage for 60 days. Exposure to NiO NPs induced marked reproductive toxicity in male rats that was manifested by increased sperm abnormalities and deterioration of sperm motility, count and viability. NiO NPs also increased lipid peroxidation and negatively affected the cellular antioxidant defense system in the testis of rats. The level of serum testosterone hormone was increased in NiO NPs-exposed rats. qPCR showed a marked downregulation in expression of steroidogenesis-related genes (CYP11A1, HSD3B and STAR) and a significant upregulation in expression of apoptosis-related gene (caspase-9) in testicular tissue of rats. Various pathological lesions and an increase in the number of PCNA-positive immune-reactive cells were also noticed in the testis of NiO NPs-exposed rats. Co-administration of HSP significantly ameliorated most of the NiO NPs-induced testicular damages and improved male fertility in rats.
Asunto(s)
Hesperidina , Nanopartículas , Animales , Antioxidantes/farmacología , Hesperidina/farmacología , Masculino , Nanopartículas/toxicidad , Níquel , Estrés Oxidativo , Ratas , Motilidad Espermática , EsteroidesRESUMEN
Monosodium glutamate (MSG) is a major taste enhancer that is used as a food additive. Vitamin C (Vit C) and Nigella sativa oil (NSO) are known for their potent antioxidant activities. OBJECTIVE: This study investigates the adverse effect of MSG on the thyroid gland and cerebellum of adult male albino rats and the protection against MSG-mediated toxicity provided by Vit C and NSO. DESIGN: Fifty rats were divided into five groups that were treated via oral gavage. Group I (control) rats received distilled water, Group II rats were treated with MSG (6 mg/gm body weight/day), Group III rats were treated with MSG and Vit C (100 mg/kg body weight /day), Group IV rats were treated with MSG and NSO (50 mg/kg body weight two times per week), and Group V rats were treated with MSG together with both Vit C and NSO with MSG. After 60 days of treatment, rats were euthanized and histological sections were prepared from the thyroid gland and the cerebellum for routine staining and immunohistochemical detection of glial fibrillar acidic protein (GFAP), Caspase-3 and proliferating cell nuclear antigen (PCNA), respectively. Cerebellar tissue was also evaluated to determine glutathione (GSH) and malondialdehyde (MDA) levels; GSH was also measured in thyroid tissue. Serum levels of fT3, fT4 and TSH (thyroid stimulating hormone) were also evaluated. RESULTS: Microscopic examination of cerebellar tissues revealed significant cerebellar injury and cellular apoptosis among the rats in Group II. The thyroid glands of Group II rats were notable for degenerating follicles, loss of colloid, sloughed follicular cells and congested blood vessels. The cerebellar and thyroid tissues from rats in treatment Groups III, IV and V revealed significantly less pathology. Cerebellar and thyroid tissues from Group II rats that were treated with MSG alone revealed intense GFAP and caspase-3 (cerebellar) and PCNA (thyroid) immunoreactivity. Furthermore, cerebellar tissues from rats received MSG alone (Group II) were notable for decreased levels of GSH and increased levels of MDA; thyroid tissue from rats in Group II also demonstrated decreased levels of GSH. Likewise, serum fT3 and fT4 levels were significantly decreased, while serum TSH was significantly increased among rats in Group II. Combined administration of Vit C and NSO together with MSG (Group V) revealed some variations in oxidative parameters compared to those in the Group I control rats. CONCLUSIONS: Oral intake of MSG resulted in degenerative changes in neurons and astrocytes in cerebellum and, also degeneration of the thyroid glands of albino rats. Concomitant administration of Vit C and NSO may limit MSG-induced damage to the cerebellum and thyroid glands and thereby provide significant protection against the oxidative damage induced by MSG.