Acute exposure to boron in Nile tilapia (Oreochromis niloticus): Median-lethal concentration (LC50), blood parameters, DNA fragmentation of blood and sperm cells.

Recently, Boron (B) contamination of aquatic ecosystem has received considerable critical attention due to its toxic effects at high concentrations on plants as well as animals. Previous studies on toxic effects of B have not dealt with DNA damages in blood and sperm cells of Nile tilapia (Oreochromis niloticus), together with blood parameters. This study consisted of two successive experiments purposes to determine these findings, including the median-lethal concentration (LC50) of B for Nile tilapia. In the first one, at 96 h, LC50 of B for Nile tilapia was 141.42 mg L-1 B. In the second one, Nile tilapia were treated with five elevated B concentrations (1, 5, 25, 50 and 100 mg L-1 B) and hematological, serum biochemical parameters, and DNA damages of Nile tilapia in these treatments were determined comparing with the control after 14 days of exposure. Hematological parameters (red blood cell count, hematocrit, and hemoglobin) were similar to each other in all groups while serum biochemical parameters (glucose, total protein, cholesterol, alkaline phosphatase, glutamic oxaloacetic transaminase, and glutamic pyruvic transaminase) in B treatments, especially in 50 and 100 mg L-1 B groups, were found significantly higher (P < 0.05). DNA fragmentation was detected in all blood cells in ≥25 mg L-1 B treatments, while all sperm cells in 100 mg L-1 B treatments. These results demonstrated the harmful effects of B at high concentration (50 and 100 mg L-1 B) on the DNA integrity of blood and sperm cells, and also the serum biochemical parameters.

Dietary olive leaf (Olea europea L.) extract alters some immune gene expression levels and disease resistance to Yersinia ruckeri infection in rainbow trout Oncorhynchus mykiss.

The aim for the present study was to investigate the effects of olive leaf (Olea europea L.) extract (OLE) on the control of Yersinia ruckeri infection in rainbow (Oncorhynchus mykiss) trout and to assess the impact on the expression of immune-related genes in the spleen and serum biochemical parameters of rainbow trout. Five experimental diets were prepared by adding 0.0%, 0.1%, 0.25%, 0.50% and 1.0% of OLE. Each diet was fed to triplicate groups of fish (mean body weight 51.22 ±â€¯3.04 g) twice a day (at 09:00 and 17:00 h) for 60 days. The dietary supplementation of OLE did not affect growth performance and feed utilization (P > 0.05). Major changes due to graded levels of OLE in the diets were observed in blood biochemical parameters (P < 0.05). TNFα, IL1-ß and IL-8 gene expressions were significanlty up-regulated in OLE 0.1% group compared with others (P < 0.05). Also, diet supplemented with OLE reduced mortality in rainbow trout fed with OLE 0.1% added diet. Present study suggests that OLE especially at 0.1% added feed may effectivelly enhance the serum biochemical parameters, survival rate and immune gene expression in rainbow trout.

In vivo assessment of polydatin, a natural polyphenol compound, on arsenic-induced free radical overproduction, gene expression, and genotoxicity.

Arsenic (As) is a well-known contaminant of global groundwater. Its exposure causes several hazardous effects on animals and human via oxidative stress. The present study examined the effect of polydatin (PD) on free radical overproduction in rats exposed to As. Thirty-five male rats randomly allocated into five equal groups. To the control group, physiological saline was given orally and to the second group only 100 mg/L As was given by drinking water for 60 days. The other groups were treated with As (100 mg/L) and PD orally at 50, 100, and 200 mg/kg/day, respectively. Treatment with As enhanced malondialdehyde level but decreased glutathione level in blood, liver, kidney, brain, lung, and heart of rats. Also, As decreased superoxide dismutase and catalase activities of erythrocyte, liver, kidney, brain, lung, and heart in rats. Furthermore, As treatment gave rise to increased DNA damage and gene expressions of interleukin 1 beta (IL-1ß), nuclear factor kappa beta (NFκB), p53, and tumor necrosis factor-α (TNF-α) in the lung, brain, kidney, and liver. However, treatment of PD ameliorated As-exposed lipid peroxidation, antioxidant enzymes activities, DNA damage, gene expressions, and histopathological changes in tissues. In conclusion, PD has a dose-dependent protective effect on lipid peroxidation and antioxidant defense mechanism in rats against As exposure.

Taurine alleviates malathion induced lipid peroxidation, oxidative stress, and proinflammatory cytokine gene expressions in rats.

The present study was considered to evaluate the protective effect of taurine on malathion-induced toxicity in rats. Totally, 48 male rats were divided into 6 equal groups: 0.5ml physiological salt solution was given orally to control rats. 0.5ml corn oil was given orally to rats in corn oil group. Malathion at dose of 27mg/kg (1/50 of LD50) was dissolved in 0.5ml corn oil and given to orally rats in malathion group. The other groups; malathion (27mg/kg) and taurine (dissolved in 0.5ml physiological salt solution) at dose of 50, 100, and 200mg/kg were given orally to rats for 30days, respectively. Malathion treatment decreased acetylcholinesterase levels in serum (30%) and liver (25%) compared to the control group. Malathion resulted in a significant increase in malondialdehyde levels whereas decreased glutathione levels, superoxide dismutase, and catalase activities in rats. Also, IF-γ, IL1-ß, TNF-α, and NFĸB mRNA expression levels were found to be increased 5, 1.7, 2.3, and 2.5 fold in malathion treated rats compared to control, respectively. However, treatment of taurine, in a dose-dependent manner, resulted in a reversal of malathion-induced lipid peroxidation, antioxidant enzyme activities, and mRNA expression levels of proinflammatory cytokines. Moreover, taurine demonstrated preventive action against malathion-induced histopathological changes in rat tissues. In conclusion, taurine exhibited a protective effect in rats against malathion-induced lipid peroxidation, besides it ameliorated antioxidant status, decreased mRNA expression levels of proinflammatory cytokine and repaired rat tissues.