Vitamin C modulates cadmium-induced hepatic antioxidants' gene transcripts and toxicopathic changes in Nile tilapia, Oreochromis niloticus.

Cadmium (Cd) is one of the naturally occurring heavy metals having adverse effects, while vitamin C (L-ascorbic acid) is an essential micronutrient for fish, which can attenuate tissue damage owing to its chain-breaking antioxidant and free radical scavenger properties. The adult Nile tilapia fish were exposed to Cd at 5 mg/l with and without vitamin C (500 mg/kg diet) for 45 days in addition to negative and positive controls fed with the basal diet and basal diet supplemented with vitamin C, respectively. Hepatic relative mRNA expression of genes involved in antioxidant function, metallothionein (MT), glutathione S-transferase (GST-α1), and glutathione peroxidase (GPx1), was assessed using real-time reverse transcription polymerase chain reaction (RT-PCR). Hepatic architecture was also histopathologically examined. Tilapia exposed to Cd exhibited upregulated antioxidants' gene transcript levels, GST-⍺1, GPx1, and MT by 6.10-, 4.60-, and 4.29-fold, respectively. Histopathologically, Cd caused severe hepatic changes of multifocal hepatocellular and pancreatic acinar necrosis, and lytic hepatocytes infiltrated with eosinophilic granular cells. Co-treatment of Cd-exposed fish with vitamin C overexpressed antioxidant enzyme-related genes, GST-⍺1 (16.26-fold) and GPx1 (18.68-fold), and maintained the expression of MT gene close to control (1.07-fold), averting the toxicopathic lesions induced by Cd. These results suggested that vitamin C has the potential to protect Nile tilapia from Cd hepatotoxicity via sustaining hepatic antioxidants' genes transcripts and normal histoarchitecture.

Oxidative stress and immunotoxic effects of lead and their amelioration with myrrh (Commiphora molmol) emulsion.

The possible role of Commiphora molmol emulsion (CME) in protecting against lead (PbAc)-induced hepatotoxicity, oxidative stress and immunotoxicity in rabbits was assessed. Six groups of animals were used: groups I (control) and II (PbAc) were not supplemented with CME. Groups III (CME50) and IV (CME50+PbAc) were administered with CME in a dose rate of 50mg/kg bwt, while groups V (CME100) and VI (CME100+PbAc) were received 100mg CME/kg bwt daily p.o for successive 14 weeks. Groups II, IV and VI were given 80 mg PbAc/kg bwt/day orally for 6 weeks starting from the 9th week. At the 12th week, animals were subjected to immunization by a single dose of sheep RBCs. The PbAc-group showed 220% increase in hepatic malondialdehyde levels, while glutathione, glutathione s-transferase and glutathione peroxidase levels decreased. Lead-acetate induced hypoproteinemia and hypoalbuminemia, and increased aminotransferases activity. It reduced the values of lymphocyte transformation test, phagocytic activity, phagocytic index and antibody titer against sheep SRBCs. Interestingly, pretreatment with CME attenuated these adverse effects in a dose-dependent protection. CME, therefore, is a potent antioxidant, and can protect against PbAc-induced hepatic oxidative damage and immunotoxicity by reducing lipid peroxidation and enhancing the antioxidant and immune defense mechanisms.

Effect of dietary zinc deficiency on rat lipid concentrations.

OBJECTIVE: Evaluation of the lipid profile in serum, liver, and testis of rats fed marginal and severe zinc deficient diets. METHODS: Three groups of rats were treated for 8 weeks with normal diet, marginally zinc deficient diet and severely zinc deficient diet. Lipid concentrations were measured in serum, liver, and testis of these groups. RESULTS: The concentrations of serum lipids were not significantly altered between marginally zinc deficient diet treated and control rats. However, in rats treated with severely zinc deficient diet, the concentrations of serum total cholesterol, high density lipoprotein cholesterol and phospholipids were significantly increased (P < 0.01) and (P < 0.001), whereas the concentration of triacylglycerol was significantly decreased (P < 0.01). However, low-density lipoprotein cholesterol concentration was non-significantly different from controls. The concentrations of liver total cholesterol, triacylglycerol and phospholipids were significantly decreased (P < 0.001) in rats treated with severely zinc deficient diet. The testicular concentration of total cholesterol was increased but this increase was non-significantly different from controls, whereas the testicular concentrations of triacylglycerol and phospholipids were significantly decreased (P < 0.001) in rats treated with severely zinc deficient diet. CONCLUSION: These results suggest that a marginally zinc deficient diet does not play a significant role in altering rat lipid concentrations. However, the changes in serum lipid concentrations could be related to those changes in tissue lipid concentrations.

Inhibition and recovery of maternal and fetal cholinesterase enzymes following a single oral dose of chlorpyrifos in rats.

Pregnant Sprague-Dawley rats (14-18 days of gestation) were treated with a single dose of 50 mg/kg (61% of oral LD50 in female rats) of chlorpyrifos ( 0,0-diethyl- 0-3,5,6-trichloro-2-pyridyl phosphorothioate) by oral gavage. Animals treated on day 18 of gestation were sacrificed at 1, 2, 4, 12 h after dosing. Animals treated on days 17, 16, 15, and 14 of gestation were sacrificed at 24, 48, 72, and 96 h after dosing, respectively. Maternal and fetal brain acetylcholinesterase (AchE) and plasma butyrylcholinesterase (BuChE) activities were significantly inhibited 1 h after treatment. Activity of fetal brain AChE and plasma BuChE recovered faster than that of the maternal enzymes. Peak inhibition of maternal spinal cord AChE and BuChE activities occurred 2 h and 1 h after dosing, respectively. Maternal spinal cord BuChE activity was totally recovered by 96 h compared to the partial recovery of spinal cord AChE activity. Maternal liver BuChE activity was significantly decreased within 1 h of dosing. The individual molecular forms (10S and 4S) of maternal and fetal brain AChE and BuChE activities were significantly decreased 1 h after treatment. Recovery of both forms of fetal brain AChE activity was much faster than the maternal forms. Activity of the 10S form of maternal control brain AChE was significantly higher than in the fetus control. The rapid recovery of cholinesterase enzymes in the fetus is attributed to the de novo synthesis of AChE enzymes in the fetus compared to the mother.