Di (2-ethylhexyl) phthalate alters neurobehavioral responses and oxidative status, architecture, and GFAP and BDNF signaling in juvenile rat's brain: Protective role of Coenzyme10.

Di-(2-ethylhexyl) phthalate (DEHP), a phthalate plasticizer, is widely spread in the environment, presenting hazards to human health and food safety. Hence, this study examined the probable preventive role of coenzyme10 (CQ10) (10 mg/kg.b.wt) against DEHP (500 mg/kg.wt) - induced neurotoxic and neurobehavioral impacts in juvenile (34 ± 1.01g and 3 weeks old) male Sprague Dawley rats in 35-days oral dosing trial. The results indicated that CQ10 significantly protected against DEHP-induced memory impairment, anxiety, depression, spatial learning disorders, and repetitive/stereotypic-like behavior. Besides, the DEHP-induced depletion in dopamine and gamma amino butyric acid levels was significantly restored by CQ10. Moreover, CQ10 significantly protected against the exhaustion of CAT, GPx, SOD, GSH, and GSH/GSSG ratio, as well as the increase in malondialdehyde, Caspas-3, interleukin-6, and tumor necrosis factor-alpha brain content accompanying with DEHP exposure. Furthermore, CQ10 significantly protected the brain from the DEHP-induced neurodegenerative alterations. Also, the increased immunoexpression of brain-derived neurotrophic factor, not glial fibrillary acidic protein, in the cerebral, hippocampal, and cerebellar brain tissues due to DEHP exposure was alleviated with CQ10. This study's findings provide conclusive evidence that CQ10 has the potential to be used as an efficient natural protective agent against the neurobehavioral and neurotoxic consequences of DEHP.

Bee venom (Apis mellifera L.) rescues zinc oxide nanoparticles induced neurobehavioral and neurotoxic impact via controlling neurofilament and GAP-43 in rat brain.

This study investigated the possible beneficial role of the bee venom (BV, Apis mellifera L.) against zinc oxide nanoparticles (ZNPs)-induced neurobehavioral and neurotoxic impacts in rats. Fifty male Sprague Dawley rats were alienated into five groups. Three groups were intraperitoneally injected distilled water (C 28D group), ZNPs (100 mg/kg b.wt) (ZNPs group), or ZNPs (100 mg/kg.wt) and BV (1 mg/ kg.bwt) (ZNPs + BV group) for 28 days. One group was intraperitoneally injected with 1 mL of distilled water for 56 days (C 56D group). The last group was intraperitoneally injected with ZNPs for 28 days, then BV for another 28 days at the same earlier doses and duration (ZNPs/BV group). Depression, anxiety, locomotor activity, spatial learning, and memory were evaluated using the forced swimming test, elevated plus maze, open field test, and Morris water maze test, respectively. The brain contents of dopamine, serotonin, total antioxidant capacity (TAC), malondialdehyde (MDA), and Zn were estimated. The histopathological changes and immunoexpressions of neurofilament and GAP-43 protein in the brain tissues were followed. The results displayed that BV significantly decreased the ZNPs-induced depression, anxiety, memory impairment, and spatial learning disorders. Moreover, the ZNPs-induced increment in serotonin and dopamine levels and Zn content was significantly suppressed by BV. Besides, BV significantly restored the depleted TAC but minimized the augmented MDA brain content associated with ZNPs exposure. Likewise, the neurodegenerative changes induced by ZNPs were significantly abolished by BV. Also, the increased neurofilament and GAP-43 immunoexpression due to ZNPs exposure were alleviated with BV. Of note, BV achieved better results in the ZNPs + BV group than in the ZNPs/BV group. Conclusively, these results demonstrated that BV could be employed as a biologically effective therapy to mitigate the neurotoxic and neurobehavioral effects of ZNPs, particularly when used during ZNPs exposure.

Palliative effect of Moringa olifera-mediated zinc oxide nanoparticles against acrylamide-induced neurotoxicity in rats.

Repeated acrylamide (ACR) exposure in experimental animals and humans causes variable degrees of neuronal damage. Because of its unique features, several green synthesized nanomaterials are explored for neuromodulatory activity. Hence, this study investigated the effect of green synthesized zinc oxide nanoparticles using Moriga olifera leaves extract (MO-ZnONP) against acrylamide (ACR)-induced neurobehavioral and neurotoxic impacts in rat. Forty male Sprague Dawley rats were distributed into four groups orally given distilled water, MO-ZnONP (10 mg/kg b.wt), ACR (20 mg/kg b.wt), or MO-ZnONP + ACR for 60 days. Gait quality and muscular, motor, and sensory function were assessed. Acetylcholinesterase (AChE), dopamine, catalase, malondialdehyde (MDA), and Zn brain contents were determined. Brain histopathology and immunohistochemical localization of the amyloid-ß protein and abnormal Tau were performed. The results revealed that MO-ZnONP significantly reduced ACR-induced sensory dysfunctions, hind limb abnormality, and motor deficits. Additionally, the ACR-induced increase in dopamine and AChE were significantly supressed by MO-ZnONP. Besides, MO-ZnONP significantly restored catalase and Zn content but reduced increased MDA brain content resulting from ACR. Furthermore, the ACR-induced neurodegenerative changes and increased amyloid-ß and phosphorylated Tau immunoexpression was significantly abolished by MO-ZnONP. Conclusively, MO-ZnONP could be used as a biologically effective compound for mitigating ACR's neurotoxic and neurobehavioral effects.

Neurobehavioral and immune-toxic impairments induced by organic methyl mercury dietary exposure in Nile tilapia Oreochromis niloticus.

Although substantial knowledge of mercury toxicity in fish has been assembled; until now, studies investigating the toxic impacts in Nile tilapia (Oreochromis niloticus) following dietary exposure to organic methyl mercury (MeHg) are less prolific. Accordingly, the current study aimed to evaluate the impacts of MeHg on neurobehavioral and immune integrity in Nile tilapia after dietary exposure. Two hundred and twenty-five juvenile Nile tilapia (19.99 ± 0.33 g) were allocated into five groups in triplicates (15 fish/replicate). G1, G2, G3, G4, and G5. O. niloticus were fed corresponding basal diets containing 0, 0.5, 1, 1.5, and 2 mg/kg diet MeHg chloride (MeHgCl) daily for 30 days, zero value represented the control G1 group. The results showed that MeHg induced significant alterations in O. niloticus behavior, the swimming behavior was significantly decreased, while scratching, biting, and fin tugging behaviors were significantly augmented. Moreover; chasing, mouth pushing, and butting behaviors were significantly increased in all the exposed groups. MeHg significantly decreased brain acetylcholine esterase (AChE) and serum immunoglobulin M (IgM) levels in all the exposed groups. Meanwhile, serum levels of lysozyme (LYZ), nitric oxide (NO), superoxide dismutase (SOD) malondialdehyde (MDA), protein carbonyl (PCO), and 8 hydroxy 2 deoxyguanosine (8OH2dG) were significantly elevated in all the exposed groups except for serum reduced glutathione (GSH) content was significantly decreased implying oxidative stress (OS), lipid peroxidation (LPO), protein, DNA damage and impaired immune response of the exposed tilapia. MeHg significantly altered transcriptional expression of immune-related genes including (TNF-α, IL-1ß, and IL-8, and IL-10) in all the exposed groups. From the obtained outcomes, the present research is the premier to investigate that dietary MeHg exposure in O. niloticus significantly induced neurobehavioral and immune defense impairments in a dose-related manner. This study exhibits that dietary MeHg may pose a potential threat to the O. niloticus populations.

Curcumin mitigates neurotoxic and neurobehavioral changes of gentamicin and sodium salicylate in rats by adjusting oxidative stress and apoptosis.

Currently, antibiotics and salicylates are the most highly consumed medications worldwide. The side effects of these pharmaceuticals on the nervous system have been little investigated. Thus, this study aimed to examine the influence of the gentamicin (GM) and sodium salicylates (SS) on neurobehavioral functions, including locomotors function, memory, and sensorimotor functions together with gamma-aminobutyric acid (GABA) neurotransmitter levels. Also, oxidative stress, lipid peroxidation, and apoptotic indicators of brain tissue were assessed. Additionally, the histopathological architecture of brain tissues was investigated. This study also evaluated the curcumin (CUR) efficacy to counteract the GM or SS induced neurotoxic impacts in rats. For this purpose, seven groups were administered physiological saline (1 ml/rat; orally), olive oil (1 ml/rat; orally), CUR (50 mg/kg bwt; orally), GM (120 mg/kg bwt; intraperitoneally), SS (300 mg /kg bwt; intraperitoneally), CUR + GM, or CUR + SS for consecutive 15 days. The results revealed that GM and SS exposure evoked impaired memory, sensorimotor deficit functions, and depressive-like behavior together with the depletion of GABA. GM and SS exposure elevated malondialdehyde and Caspase-3 levels, but total antioxidant capacity and Bcl-2 levels were reduced. Besides, GM and SS exposure induced distinct pathological perturbations in cerebral cortices and hippocampus tissues. CUR significantly reversed the GM and SS harmful impacts. In conclusion, these findings verified that CUR could be a biologically efficient protective intervention against GM and SS induced neurotoxic impacts and neurobehavioral aberrations.

Changing dietary n-6:n-3 ratio using different oil sources affects performance, behavior, cytokines mRNA expression and meat fatty acid profile of broiler chickens.

Typical formulated broiler diets are deficient in n-3 poly-unsaturated fatty acids (PUFA) due to widening n-6:n-3 PUFA ratio which could greatly affect performance, immune system of birds and, more importantly, meat quality. This study was conducted to evaluate the effect of modifying dietary n-6:n-3 PUFA ratio from plant and animal oil sources on performance, behavior, cytokine mRNA expression, antioxidative status and meat fatty acid profile of broiler chickens. Birds (n = 420) were fed 7 diets enriched with different dietary oil sources and ratios as follows: sunflower oil in control diet (C); fish oil (FO); 1:1 ratio of sunflower oil to FO (C1FO1); 3:1 ratio of sunflower oil to fish oil (C3FO1); linseed oil (LO); 1:1 ratio of sunflower oil to linseed oil (C1LO1); 3:1 ratio of sunflower oil to linseed oil (C3LO1), resulting in dietary n-6:n-3 ratios of approximately 40:1, 1.5:1, 4:1, 8:1, 1:1, 2.5:1 and 5:1, respectively. The best final body weight, feed conversion ratio as well as protein efficiency ratio of broilers were recorded in the C1FO1 and C1LO1 groups. Compared with the control group, the dressing percentage and breast and thigh yield were highest in the C1FO1 and C1LO1 groups. Narrowing the dietary n-6:n-3 ratio increased (P < 0.05) n-3 PUFA content of breast meat. Moreover, the breast meat contents of eicosapentaenoic acid and docosahexaenoic acid increased (P < 0.05) with increasing dietary FO whereas α-linolenic acid content was higher with LO supplementation. Also, enriching the diets with n-3 PUFA from FO and LO clearly decreased (P < 0.05) serum total cholesterol, triglycerides and very low-density lipoproteins and enhanced antioxidative status. The feeding frequency was decreased (P < 0.05) in the C1FO1 and C1LO1 groups. Likewise, n-3 PUFA-enriched diets enhanced the frequency of preening, wing flapping and flightiness. Animal oil source addition, compared to plant oil, to broiler diets enhanced the relative mRNA expression of interferon gamma, interleukin-1 beta, interleukin-2 and interleukin-6 genes, especially at low n-6:n-3 ratios. This study has clearly shown that narrowing n-6:n-3 ratio through the addition of FO or LO improved performance and immune response of broilers and resulted in healthy chicken meat, enriched with long chain n-3 PUFA.