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Moreover, therapeutic combination or association possibilities targeting purinergic system components are also suggested as a possible useful tool to be tested in future researches, aiming to unveil a novel option to treat COVID-19 patients.The night shift paradigm induces a state of chronic partial sleep deprivation (CPSD) and enhances the vulnerability to neuronal dysfunction. However, the specific neuronal impact of CPSD has not been thoroughly explored to date. In the current study, the night shift condition was mimicked in female Swiss albino mice. The classical sleep deprivation model, i.e., Modified Multiple Platform (MMP) method, was used for 8 h/day from Monday to Friday with Saturday and Sunday as a weekend off for nine weeks. Following nine weeks of night shift schedule, their neurobehavioral profile and physiological parameters were assessed along with the activity of the mitochondrial complexes, oxidative stress, serotonin levels, and inflammatory markers in the brain. Mice showed an overall hyperactive behavioral profile including hyperlocomotion, aggression, and stereotyped behavior accompanied by decreased activity of mitochondrial enzymes and serotonin levels, increased oxidative stress and inflammatory markers in whole brain homogenates. Collectively, the study points towards the occurrence of a hyperactive behavioral profile akin to mania and psychosis as a potential consequence of CPSD.Copper (Cu) is an essential micronutrient for both humans and animals; however, excessive intake of Cu can be immunotoxic. There are limited studies on spleen toxicity induced by Cu. This study was conducted to investigate the effects of Cu on spleen oxidative stress, apoptosis, and inflammatory responses in mice orally administered with 0 mg/kg, 10 mg/kg, 20 mg/kg, and 40 mg/kg of CuSO4 for 42 days. As discovered in this work, copper sulfate (CuSO4) reduced the activities of antioxidant enzymes (SOD, CAT, and GSH-Px), decreased GSH contents, and increased MDA contents. Meanwhile, CuSO4 induced apoptosis by increasing TUNEL-positive cells in the spleen. Also, CuSO4 increased the expression of γ-H2AX, which is the marker of DNA damage. Concurrently, CuSO4 caused inflammation by increasing the mRNA levels of interleukin-1β (IL-1β), IL-2, IL-4, IL-6, IL-12, tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ). In conclusion, the abovementioned findings demonstrate that over 10 mg/kg CuSO4 can cause oxidative stress, apoptosis, DNA damage, and inflammatory responses, which contribute to spleen dysfunction in mice.Cadmium (Cd) poisoning in humans and fish represents a significant global problem. Bacillus cereus (B. cereus) is a widely used probiotic in aquaculture. The objective of this study was to evaluate the potential of B. cereus in ameliorating Cd-induced toxicity in mirror carp. The biosorption rate of Zn for the B. cereus in 85.99% was significantly more than five strains. All fishes were exposed for 30 days to dietary ZnCl2 (30mg/kg), waterborne Cd (1 mg/L), and/or dietary Zn-enriched B. cereus (Zn 30mg/kg and 107cfu/g B. cereus). At 15 and 30 days, the fishes were sampled, and bioaccumulation, antioxidant activity, and intestinal microbiota were measured. Waterborne Cd exposure caused marked alterations in the composition of the microbiota. MCT inhibitor Dietary supplementation with Zn-enriched B. cereus can reduce the changes in the composition of intestinal microbiota in Cd exposure and decrease the pathogenic bacteria of Flavobacterium and Pseudomonas in Zn-enriched B. cereus groups. The results obtained indicate that Zn-enriched B. cereus can provide a significant protective effect on the toxicity of cadmium by inhibiting alterations in the levels of bioaccumulation and antioxidant enzyme including superoxide dismutase (SOD), catalase (CAT), total antioxidant (T-AOC), and malonaldehyde (MDA). Our results suggest that administration of Zn-enriched B. cereus has the potential to combat Cd toxicity in mirror carp.This study aimed to consider the oxidative damage induced by cadmium (Cd) and apoptosis and the role of N-acetylcysteine (NAC) in preserving hepatic cells against Cd toxicity. Male rats were randomly divided into seven groups including G1 (control), G2 (single dose of Cd), G3 (continuous dose of Cd), G4 (single dose of Cd + continuous dose of NAC), and G5 (continuous dose of Cd + continuous dose of NAC). Hepatic cells apoptosis was measured using TUNEL assay method. Levels of malondialdehyde (MDA), TNF-α, IL-10, and total antioxidant capacity (TAC) were measured by specific kits. Expression of c-myc and Ask-1 genes was considered using RT-PCR. NAC treatments significantly improved TAC and IL-10, but decreased MDA and TNF-α values in rats that were exposed to a single and continuous dose of Cd (p less then 0.05). Exposure to a single and continuous dose of Cd caused a significant increase in c-myc expression by 3.76-fold (p less then 0.001) and 8.17-fold (p less then 0.0001), respectively. Single and continuous dose treatment of Cd led to a significant increase in Ask1 expression by 4.38-fold (p less then 0.001) and 13.52-fold (p less then 0.001), respectively. NAC treatments significantly decreased the expression of c-myc, and Ask-1 in rats exposed to single or continuous Cd. Cd exposure is strongly associated with oxidative stress, inflammation, antioxidant depletion, and liver cells apoptosis. NAC can protect liver tissue against Cd by elevating antioxidants capacity, mitigating oxidative stress and inflammation, as well as down-regulating of apoptotic genes.Gene expression can be modulated by epigenetic modifications, which may lead to a rapid adaptation to environmental stress. After stress cessation, changes in gene expression could be reversed, which would allow organisms to maintain their phenotype under transient environments, but this mechanism is poorly understood. Social stress downregulates a gene directly involved in pheomelanin synthesis (Slc7a11) by changing DNA m5C levels, avoiding cellular damage caused by stress. We thus investigated if Slc7a11 expression is reversed in melanocytes of growing flank feathers to avoid changes in the pigmentation phenotype. We measured the expression level of Slc7a11 at three time points before stress exposure, immediately after stress exposure and six weeks after stress cessation in 37 male zebra finches (Taeniopygia guttata). No differences in Slc7a11 expression were detected between birds exposed to stress and controls six weeks after stress elimination, indicating that stress removal led to a cessation of Slc7a11 downregulation.