Growth, carcass characteristics, meat quality, and microbial aspects of growing quail fed diets enriched with two different types of probiotics (Bacillus toyonensis and Bifidobacterium bifidum).

The present investigation aimed to explore the impact of dietary graded levels of 2 types of probiotic bacteria (Bacillus toyonensis [BT] and Bifidobacterium bifidum [BB]) on growth, carcass traits, meat quality, and bacteriology of growing Japanese quail reared under the cage system. One thousand three hundred sixty Japanese quail day-old chicks were randomly divided into 10 groups (8 replicates each). Birds were fed a basal diet (control, T1) and the basal diet plus 0.05, 0.075, 0.10, and 0.125% BT (T2, T3, T4, and T5, respectively), 0.10% BB (T6), and the same previous doses of BT plus 0.05% BB (T7, T8, T9, and T10, respectively). Results showed a significant (P < 0.001) increase in final BW and weight gain because of probiotic supplementation (except T2 for weight gain). Both feed intake and feed conversion ratio did not differ during the overall experimental period (1-42 D of age) except feed intake that was reduced in T2 and increased in T5 and T9 groups. All carcass traits studied were significantly (P < 0.01) affected by probiotics, and the combination between BT and BB in group T8 increased all studied parameters as compared with the other treatment groups. The quail meat color of redness a∗ and L∗ values, thiobarbituric content, cooking loss, proteolysis, and total coliform were decreased (P < 0.001) by probiotic treatment. In general, supplementing BT, BB, or their combination to the basal diet delayed the proliferation of pathogenic bacteria in the diet and intestine. Using BT and BB as feed supplements enhanced growth performance and meat quality of quails as well as diminished pathogenic bacteria proliferation in their diet and intestine. As per our results, we can recommend the application of T5 and T8 to T10 levels for the best performance, carcass traits, and meat quality of growing quails.

Role of thymoquinone and ebselen in the prevention of sodium arsenite-induced nephrotoxicity in female rats.

The aim of this study is to investigate the protective effects of thymoquinone (TQ) and ebselen (Eb) on arsenic (As)-induced renal toxicity in female rats. Sodium arsenite was orally administrated at a dose of 20 mg/kg body weight daily for 28 days, either alone or 1 h before TQ (10 mg/kg) or Eb (5 mg/kg) administration. Renal tissue As concentration and oxidative stress markers, including lipid peroxidation (LPO), nitrite/nitrate, and glutathione (GSH) levels, were determined. In addition to the oxidative stress response, antioxidant enzyme activities including that of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase were measured. Exposure to As elicited a significant increase in As concentration and significant modifications to the redox state of the kidney, as was evidenced by a significant elevation in LPO and nitrite/nitrate concentration, with a concomitant reduction in GSH content and antioxidant enzyme activity. The oxidant/antioxidant imbalance observed in As toxicity was associated with a significant elevation in renal tumor necrosis factor α, interleukin 6, B-cell lymphoma 2 (Bcl-2)-associated X protein, and caspase 3 levels, in addition to a significant decrease in Bcl-2 levels. Post-administration of TQ and Eb markedly prevented As-induced oxidative stress, inflammation, apoptosis, and As accumulation in the renal tissue and reduced histological renal damage. These findings demonstrate that TQ, the main bioactive phytochemical constituent of Nigella sativa seed oil, and Eb, an organoselenium compound, could significantly inhibit As-induced oxidative damage, apoptosis, and inflammation, and significantly attenuate the accumulation of As in renal tissues by facilitating As biomethylation and excretion.

Radioprotection of 1,2-dimethylhydrazine-initiated colon cancer in rats using low-dose γ rays by modulating multidrug resistance-1, cytokeratin 20, and ß-catenin expression.

Ionizing radiation is a widely used therapy for solid tumors. However, high-dose ionizing radiation causes apoptosis, transforms normal cells into tumor cells, and impairs immune functions, leading to the defects in the removal of damaged or tumor cells. In contrast, low-dose radiation has been reported to exert various beneficial effects in cells. This experimental study investigated the effect of γ rays at low dose on the development of colorectal tumor in a 1,2-dimethylhydrazine (DMH)-induced colon cancer. Colorectal tumor model was induced in Wistar rats by subcutaneous injection of DMH (20 mg/kg) once a week for 15 weeks. Starting from zero day of DMH injection, a single low dose of whole-body γ irradiation of 0.5 Gy/week was applied to the rats. A significant reduction in lipid peroxidation, nitric oxide, and elevation in the glutathione content and antioxidant enzyme activity (superoxide dismutase and catalase) were observed after γ irradiation comparing with DMH group. Moreover, γ ray reduced the expressions of multidrug resistance 1 (MDR1), ß-catenin, and cytokeratin 20 (CK20) those increased in DMH-treated rats. However, survivin did not change with γ ray treatment. A histopathological examination of the DMH-injected rats revealed ulcerative colitis, dysplasia, anaplasia, and hyperchromasia. An improvement in the histopathological picture was seen in the colon of rats exposed to γ rays. In conclusion, the present results showed that low-dose γ ray significantly inhibited DMH-induced colon carcinogenesis in rats by modulating CK20, MDR1, and ß-catenin expression but not survivin expression.

Hepatic oxidative stress in Mongolian gerbils experimentally infected with Babesia divergens.

The present study aimed to investigate oxidative stress, DNA damage, and histopathological alterations in hepatic tissues of Mongolian gerbils experimentally infected with Babesia divergens. It was found that parasitaemia reached approximately 77% at day 5 post-infection. The liver became dark-brown and extremely friable, and hepatic sinusoids were dilated and contained macrophages and parasite-containing erythrocytes. Infection also induced inflammation and injury of the liver. This was illustrated by (1) an increase in inflammatory cellular infiltrations, (2) a decrease in total antioxidant capacity, as indicated by lowered glutathione and catalase levels, (3) increased production of nitric oxide-derived products (nitrite/nitrate) and malondialdehyde, and (4) increased lactic acid dehydrogenase activity and protein carbonyl content in the liver. Infection also interfered with the normal cell cycle of the hepatic tissue, as indicated by a significant increase in the percentage of liver cells at G0/G1 from approximately 86.2% to 97.5% and in S phases from 0.28% to 2.2%. Collectively, the present data suggest that B. divergens infection could induce cell-cycle alteration following oxidative stress and DNA damage in hepatic tissue. Further work is required to investigate the mechanism by which this hepatic tissue damage takes place.