Potential effect dietary supplementation of calcium tetraborate in quails exposed to cadmium: Its impact on productive performance, oxidative stress, cecal microflora, and histopathological changes.

Cadmium (Cd) is a ubiquitous environmental pollutant, and Cd exposure harms human health, agriculture, and animal husbandry. The present study aimed to investigate the potential protective effect of dietary supplementation of calcium tetraborate (CTB) on productive performance, oxidative stress, cecal microflora, and histopathological changes in quail exposed to Cd. A total of one hundred twenty, 6-week-old Japanese quail (four females and two males/replicate) were divided into four groups (30 quails/group): the control group (feeding basic diet), CTB group (basic diet containing 300 mg/kg CaB4O7, 22.14% elemental B/kg diet), the Cd group (basic diet containing 100 mg/kg cadmium chloride (CdCl2) (total Cd content of 92.1 mg/kg)) and the CTB + Cd group (basic diet containing 300 mg/kg CTB and 100 mg/kg CdCl2). The results showed that Cd exposure caused decreased performance, increased the proportion of broken and soft-shelled eggs, induced oxidative stress, affected cecal microflora, epicardial hemorrhages in the heart, focal necrosis in the liver, degeneration in the kidneys, and degenerated and necrotic seminiferous tubules in the testicles. CTB prevented Cd-induced oxidative stress in liver tissue by increasing total antioxidant status and reducing total oxidant status. In addition, CTB improved egg production and feed conversion ratio (FCR). CTB protected the cecal microflora by inhibiting Enterobacteriaceae and promoting Lactobacillus. CTB also reduced Cd-induced histopathological damage in the heart, liver, kidneys, and testicles. In conclusion, these findings suggest that CTB could be used in Cd-challenged quail, and this compound provides new insights into the toxicity of environmental Cd.

Potential ameliorative effect of dietary quercetin against lead-induced oxidative stress, biochemical changes, and apoptosis in laying Japanese quails.

Lead (Pb) is a widespread environmental pollutant which is a toxic threat to human and animal health. The present study was designed to evaluate the ameliorative role of quercetin in laying quails exposed to Pb. A total of 112 birds were randomly divided into four groups. The control group was fed with basal diet, the Pb group was fed with ration supplemented with Pb at the dose of 100 mg/kg (as Pb (II) acetate trihydrate), the Quercetin group was fed with ration supplemented with quercetin at the dose of 400 mg/kg, and the Pb+ Quercetin group was fed with ration supplemented with Pb at the dose of 100 mg/kg and quercetin at dose of 400 mg/kg. Results showed that serum total protein, glucose, albumin, and blood urea nitrogen (BUN) values of the Pb + Quercetin group partially improved with quercetin supplementation. Meanwhile, serum creatinine values of the Pb + Quercetin group was found to be significantly lower than that of the Pb group. Aspartate aminotransferase (AST) and alanine transaminase (ALT) enzyme activities in the Quercetin and Pb + Quercetin groups were similar to those of the Control group, unlike the Pb group. Moreover, alkaline phosphatase (ALP) enzyme activity of the Pb + Quercetin group significantly improved with the addition of quercetin. We also found that malondialdehyde (MDA) levels of the kidney, liver, and heart were significantly reduced by quercetin supplementation. The glutathione, catalase, and glutathione peroxidase activities of the kidney, liver, and heart tissue were increased by quercetin supplementation. These results were in line with the observed apoptotic markers. The expression of caspase-3 and caspase-9 were significantly decreased by quercetin supplementation. It may be concluded that dietary supplementation with quercetin ameliorates the toxic effects of Pb exposure by alleviating oxidative stress, biochemical changes, and apoptosis in quails.

The protective effect of chrysin against carbon tetrachloride-induced kidney and liver tissue damage in rats.

The aim of this study was to investigate the possible protective effects of chrysin on oxidative status and histological alterations against carbon tetrachloride (CCl4)-induced liver and kidney tissue in rats. The animals were randomly divided into four groups; the control, chrysin (100 mg/kg), CCl4 (0.5 ml/kg) and chrysin + CCl4 groups. Liver and kidney injuries were assessed by biochemical and histopathological examinations. The levels of malondialdehyde (MDA), reduced glutathione (GSH), and superoxide dismutase (SOD) activity were measured in tissues. Serum tumor necrosis factor-α (TNF-α), aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea, and creatinine levels were also measured in blood samples. MDA, serum TNF-α, AST, ALT, urea, and creatinine levels (p < 0.05) were significantly higher, and SOD activity and GSH level were significantly (p < 0.05) lower in the CCl4 group than in the control group. Treatment with chrysin in the chrysin + CCl4 group decreased MDA, AST, ALT, creatinine, and TNF-α levels (p < 0.05), and increased SOD activity, GSH levels (p < 0.05), and serum TNF-α levels (p < 0.05). In addition, body weight change (BWC) (p < 0.05) and feed intake (FI) were significantly lower (p < 0.001) in the CCl4 group than in the control group. Moreover, treatment with chrysin increased BWC and FI in the chrysin + CCl4 group compared with that in the CCl4 group. These findings also confirmed by histopathological examination. The chrysin treatment ameliorated the CCl4-induced biochemical and pathological alterations. These results demonstrated that chrysin provided amelioration on the rat liver and kidney tissues CCl4-induced injury by increasing the antioxidant activity.