Dietary exposure to methyl mercury chloride induces alterations in hematology, biochemical parameters, and mRNA expression of antioxidant enzymes and metallothionein in Nile tilapia.

Methyl mercury chloride "MMC" (CH3ClHg) is an ubiquitous environmental toxicant that causes a variety of adverse effects. In the present study, we investigated the effects of sub-chronic toxicity of MMC on Nile tilapia (Oreochromis niloticus) through the evaluation of growth performance and hematological, biochemical, and oxidative stress biomarkers. From 150 healthy fish, five equally sized treatment groups were created: a control (CT) group fed with a basal diet and four MMC treatment groups exposed to 0.5, 1, 1.5, and 2 mg of MMC per kg of basal diet for 60 days. MMC exposure significantly reduced the growth performance and survival of O. niloticus and decreased red blood cell count and hemoglobin concentration. Treated fish exhibited normocytic normochromic anemia in addition to leucopenia, lymphopenia, granulocytopenia, and monocytopenia. Moreover, MMC exposure significantly affected liver function, including a reduction in the total protein levels while increasing cholesterol and triglyceride levels. It also markedly increased the production of stress biomarkers such as glucose and cortisol levels. Furthermore, MMC significantly elevated the levels of hepatic enzymes, induced tissue damage, and caused inflammation, as indicated by the upregulation of mRNA expression of hepatic metallothionein. Finally, MMC exposure induced oxidative stress by altering the antioxidant status of the liver and downregulating the mRNA expression of superoxide dismutase, glutathione peroxidase, and glutathione S-reductase. In conclusion, MMC toxicity induced hematological and biochemical alterations, leading to an enhanced state of oxidative stress in O. niloticus.

Amelioration of fenitrothion induced oxidative DNA damage and inactivation of caspase-3 in the brain and spleen tissues of male rats by N-acetylcysteine.

N-acetylcysteine (NAC) has largely been used as an effective chemo- protective agent owing to their beneficial effect in restoring several physiological parameters and relieving oxidative stress. Interestingly, it has been suggested that NAC mechanisms of action extend beyond being a precursor to the antioxidant glutathione and that they may involve several neurotropic and inflammatory pathways. Exposure to fenitrothion, an organophosphorus insecticide, promotes oxidative stress and induces several deleterious changes in the immune response and various tissues including cerebrum and spleen. The main objective of our study was to investigate ameliorative efficacy of N-acetylcysteine for immunological and neurological alterations and oxidative DNA damage induced by fenitrothion toxicity in cerebrum and spleen tissues of male rats. Our results revealed that oral exposure to fenitrothion for 30 days caused a reduction in the erythrocyte count in addition to leukocytosis, lymphocytosis, and neutrophilia. Also, this route of administration increased the serum levels of LDH, TNF-α, and IL-2 with reduction in serum immunoglobulins (IgG & IgM) concentrations. Furthermore, a significant downregulation in the antioxidant markers (GSH & SOD) with an elevation of free radical (MDA) levels were noticed. Regarding the brain, fenitrothion administration inhibited AchE activity and increased brain GABA, serotonin and dopamine levels. Moreover, it induced an elevation in oxidative DNA damage indicated by 8-hydroxy 2-deoxyguanosine (8OH2dG) and mRNA expression of pro-apoptotic genes, including Bax, and p53, but Bcl-2 expression was reduced. N-acetylcysteine co-treatment restored the normal physiological tone in most of these parameters. Immunostaining for GFAP and Caspase-3 markers in the brain and spleen tissues were increased respectively. In conclusion, N-acetylcysteine supplementation has an ameliorative effect against immunotoxic, neurotoxic and oxidative DNA damage induced by fenitrothion exposure.

Dose-related impacts of imidacloprid oral intoxication on brain and liver of rock pigeon (Columba livia domestica), residues analysis in different organs.

Available data regarding Imidacloprid (IMI) insecticide hazards to birds are still being scare. Our study aimed to investigate toxic impacts of IMI oral gavage by different dose levels on the brain and liver of Rock pigeon (Columba livia domestica). Forty mature male birds were divided equally into four groups. A control group (C) was orally dosed Mazola corn oil and other three groups; the low dose (LD), the medium dose (MD), and the high dose (HD) groups were orally dosed IMI in Mazola corn oil by three dose levels corresponding to 1/15th, 1/10th, 1/5th IMI oral LD50 respectively. IMI exposure induced a significant decrease in serum levels of glutathione (GSH), superoxide dismutase (SOD) enzyme activity. On the other hand; malondialdehyde (MDA) levels were elevated. The levels of serum total protein, albumin, globulin, and A/G ratio showed a non-significant changes in all IMI dosed groups except levels of total protein in the HD IMI dosed group showed a significant decrease compared to the C group. Serum levels of alanine aminotransferase (ALT), lactate dehydrogenase (LDH), uric acid, plasma tumor necrosis factor α (TNFα) and plasma acetylcholinesterase (AChEs) enzyme activities showed a significant dose related increase in all IMI exposed groups compared to the C group; except the levels of ALT, LDH, and uric acid showed a non significant decrease in the LD IMI dosed group only. Residues of IMI were detected in the pectoral muscles, liver, brain, and kidney of all dosed rock pigeon. Moreover; pectoral muscles were the highest tissue for IMI residues detection. This is the first study reports accumulation of IMI in tissues other than crop, liver, and kidney of rock pigeon including brain and muscles. Moreover, the examined brain and liver tissues of all IMI dosed groups showed dosed related alterations in their structural and ultra-structural morphology. It is concluded that IMI oral administration to pigeon induced oxidative stress and detrimental effects in brain and liver of exposed pigeons. Additionally; IMI bio-accumulated in different organs being muscles is the highest tissues for IMI residues, thus monitoring of IMI residues in food is very essential.

Anti-Inflammatory, Immunomodulatory, and Antioxidant Activities of Allicin, Norfloxacin, or Their Combination against Pasteurella multocida Infection in Male New Zealand Rabbits.

The present study investigated the efficacy of allicin as an antibacterial, anti-inflammatory, antioxidant, and immunostimulant agent in reducing the severity of Pasteurella multocida (P. multocida) type B infection in rabbits. Fifty New Zealand rabbits, 5 weeks old, were divided equally into five groups. Except for group 1, all groups were intranasally infected with P. multocida type B (2 × 105 colony forming units/ml/rabbit). Then, group 3 rabbits were orally treated with allicin (50 mg/kg BW) for 5 days, group 4 rabbits received a single oral dose of norfloxacin 30% (100 mg/kg BW), while group 5 rabbits were treated with a combination of norfloxacin and allicin. Hematological, serum biochemical, inflammatory cytokine, immunological, and histopathological analyses were performed. Results revealed that rabbits, infected with P. multocida type B, exhibited macrocytic hypochromic anemia and leukocytosis with a significant elevation in the phagocytic percentage and index. Moreover, significant reductions in serum total protein, albumin, globulin, and immunoglobulin (IgG and IgM) levels were observed in infected rabbits. Infected rabbits showed significant increases in serum inflammatory cytokine (TNF-α and IL-6), alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, and serum bilirubin (total, direct, and indirect) levels. Further, P. multocida infection induced oxidative stress as demonstrated by the significant reduction in serum levels of reduced glutathione and superoxide dismutase enzyme and marked elevation in serum malondialdehyde. Treatment with allicin, norfloxacin, or their combination significantly ameliorated the alterations in all studied parameters. In conclusion, allicin could ameliorate the inflammation and oxidative stress, induced by P. multocida type B infection in rabbits.

Protective role of quercetin against hematotoxic and immunotoxic effects of furan in rats.

Furan (Fu) is a liver carcinogen produced during heating process of food and concerns a public health problem. The current study was undertaken to evaluate the protective role of quercetin (Que) on Fu-induced hematological, immunological, and histopathological alterations in rats. Fifty male Sprague Dawley rats were divided into five equal groups. Group I (Cont) received distilled water, group II (CO) received corn oil, group III (Que) received Que at 50 mg/kg BW, group IV (Fu) received Fu at 16 mg/kg BW, and group V received Que + Fu simultaneously; all groups gavaged daily for 30 days. Our results revealed that Fu administration significantly elevated RBCs, Hb, PCV, WBCs, lymphocytes, and granulocytes and reduced phagocytic percent (Ph%) and index (PhI). Fu decreased the serum total protein, albumin, globulin, IgM, IgG, and IL4, with a significant increase in the TNFα and 8-OHdG. Moreover, it decreased the GSH content and GST activity and increased the MDA levels in the splenic tissue. Histopathologically, Fu led to a moderate depletion in the lymphoid cells and weak immunostaining of CD20 antigen of few lymphocytes appeared in the spleen. Meanwhile, Que co-administration ameliorated the altered hematological parameters and improved the Ph% and PhI. It modulated the serum biochemical parameters and immunoglobulins. Moreover, it decreased lipid peroxidation and enhanced antioxidant status in the spleen. The results indicated that Que possesses antioxidant protective activity against Fu-induced oxidative damage and stimulates the immune function.

Ameliorative effect of flaxseed oil against thiacloprid-induced toxicity in rats: hematological, biochemical, and histopathological study.

The present study was carried out to evaluate the hematological, biochemical, and histopathological changes due to thiacloprid toxicity, and the potential protective role of flaxseed oil in male Wistar albino rats. Subacute thiacloprid intoxication induced a significant increase in RBCs, Hb, PCV, and WBCs count, and bone marrow micronucleus (MN) formation. Moreover, there was a significant increase in serum biochemical parameters related to hepatic injury: alanine aminotransferase (ALT) and alkaline phosphatase (ALP). Serum total protein and albumin levels were significantly reduced. Thiacloprid increases tumor necrosis factor-alpha (TNF-α) and interleukine-2(IL-2). There was a significant decrease in glutathione-S-transferase, while the lipid peroxidation (MDA) and cytochrome P450 activity were significantly increased. Flaxseed oil coadministration partially retrieved the changes in all studied parameters. Thiacloprid induced histopathological liver damage, which was minimized as a result of flaxseed oil treatment. In general, it was concluded that, flaxseed oil able to protect against thiacloprid-induced hepatoxicity.