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Oyagbemi, A. A.
- Cobalt Chloride-Induced Hepatic and Intestinal Damage in Rats: Protection by Ethyl Acetate and Chloroform fractions of Ocimum Gratissimum
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1 Department of Veterinary Physiology, Biochemistry and Pharmacology, University of Ibadan, NG
2 Department of Veterinary Medicine, University of Ibadan, NG
1 Department of Veterinary Physiology, Biochemistry and Pharmacology, University of Ibadan, NG
2 Department of Veterinary Medicine, University of Ibadan, NG
Source
Toxicology International (Formerly Indian Journal of Toxicology), Vol 23, No 1 (2016), Pagination: 38-48Abstract
Cobalt chloride is known to produce symptoms of diarrhea, vomiting and other gastrointestinal disturbances. We investigated the potential roles of the ethyl acetate and chloroform fractions of Ocimum gratissimum (OG), traditionally used to treat diarrhea and other gastrointestinal disorders in protection against cobalt chloride (CoCl2)-induced liver and intestinal damage. Wistar albino rats were given CoCl2 (350 ppm) in drinking water for 7 days, alone or concurrently with either fractions of OG at 100 and 200mg/kg each. Gallic acid (120 mg/kg) was administered to a group of rats as a standard flavonoid. Biochemical indices of oxidative stress, antioxidant enzyme activities, the levels of pro-inflammatory cytokines (Interleukin 1β; IL-1β and Tumor necrosis factor, TNF-α) were evaluated and the histological appearance of the liver and intestinal mucosa was investigated. CoCl2 produced significant elevations (p<0.05) in hydrogen peroxide (H2O2), malondialdehyde (MDA), IL-1β, alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP). This was accompanied with significant reductions (p<0.05) in reduced glutathione (GSH), glutathione peroxidase (GPX) and glutathione S-transferase (GST) activities. Liver sections of rats exposed to CoCl2 had poor architecture and areas of necrosis with several dead hepatocytes, while some appeared with hyperchromic nuclei. Intestinal mucosa showed significant loss of absorptive epithelial cells with CoCl2 exposure. Treatment with the fractions from OG produced reduction in H2O2, MDA and IL-1β levels; reduced serum activities of ALT, AST and ALP; restoration of GSH levels and improved activities of GPX and GST. The fractions significantly preserved the hepatic and intestinal architecture.Our results indicate that the fractions of OG exhibited considerable hepatic and intestinal protection by reduction in levels of oxidants and pro-inflammatory cytokines, enhancement of antioxidant enzyme activities and preservation of tissue integrity and might thus be very useful agents in protecting the liver and intestines during concurrent exposure to Cobalt chloride.Keywords
Cobalt, Hepatotoxicity, Intestines, Ocimum gratissimum, Gallic Acid, Antioxidant.
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- Concentration-Dependent Inhibition of Acetylcholinesterase by Organophosphate Poisoning in Dogs: A Biochemical and Electrocardiograph Study
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Authors
Affiliations
1 Department of Veterinary Physiology, Biochemistry and Pharmacology, University of Ibadan, NG
2 Department of Veterinary Medicine, University of Ibadan, NG
1 Department of Veterinary Physiology, Biochemistry and Pharmacology, University of Ibadan, NG
2 Department of Veterinary Medicine, University of Ibadan, NG
Source
Toxicology International (Formerly Indian Journal of Toxicology), Vol 23, No 1 (2016), Pagination: 63-72Abstract
Organophosphate poisoning (OP) is one of the most common poisonings in developing countries. In this study, twentyfour dogs in four groups of six each were used. Control group bathed with water only, group B with 16% Coumaphos (recommended), groups C and D with times 10 and 20 of 16% Coumaphos, respectively. Blood was collected from cephalic vein for biochemical assays. Electrocardiographic parameters were assessed from a Lead-II electrocardiogram. There was a significant increase (p<0.05) in total cholesterol in group B and D compared to the control. LDL-cholesterol decreased significantly (p<0.05) in all groups compared to the control. The activity of superoxide dismutase (SOD) reduced (p<0.05) significantly across all the groups and even after 36 hours of exposure. However, the activity of the glutathione peroxidase (GPx) was not affected following exposure to OP. The serum reduced glutathione (GSH) fell in a concentration dependent manner in all animals exposed to OP. Coumaphos exposure led to a significant (p<0.05) increase in serum MDA in a concentration dependent manner after 36 hours post exposure. The serum nitric oxide (NO) and MPO content increased (p<0.05) significantly following exposure to different concentrations of Coumaphos. The activity of Acetyl cholinesterase (AchE) fell significantly from the normal concentration of the OP down to the highest concentration. The activity of serum creatine phosphokinase (CK) increased (p<0.05) significantly in groups C and D compared to the control and recommended concentration. Electrocardiographic abnormalities recorded included low-voltage R-waves, first degree heart block, significant increased (p<0.05) heart rate (HR) and shortened QT interval compared to the control and recommended concentrations. Taking together, coumaphos poisoning caused an inhibition of AchE and significant potentially fatal arrhythmias via the induction of oxidative stress.Keywords
Coumaphos, Organophosphate Poisoning (OP), Electrocardiogram (ECG), Oxidative Stress, Acetylcholinesterase (AchE), Cardiotoxicity.References
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Affiliations
1 Department of Veterinary Physiology, Biochemistry and Pharmacology, University of Ibadan, NG
2 Department of Veterinary Medicine, University of Ibadan, NG
3 Department of Biochemistry, College of Medicine, University of Ibadan, NG
1 Department of Veterinary Physiology, Biochemistry and Pharmacology, University of Ibadan, NG
2 Department of Veterinary Medicine, University of Ibadan, NG
3 Department of Biochemistry, College of Medicine, University of Ibadan, NG
Source
Toxicology International (Formerly Indian Journal of Toxicology), Vol 23, No 3 (2016), Pagination: 246-253Abstract
Sixty male Wistar rats were divided into six groups of 10 rats each. Group I was the control. Group II received homocysteine (Hcy) (200 mg/kg body weight) alone daily for 14 days. Rats in groups III and IV received Kolaviron orally at 100 and 200 mg/kg respectively, in addition to Hcy. Rats in groups V and VI received Garcinia kola (GK) orally (100 and 200 mg/ kg respectively) in addition to Hcy (200 mg/kg) for a period of 14 days. The results showed that Hcy caused a reduction in heart rate, shortened QT and QTc intervals together with low voltage QRS which were reversed by Kolaviron (100&200 mg/kg body weight) and Garcinia kola (100&200 mg/kg body weight). Hcy alone also caused a significant (p<0.05) increase in MDA, H2O2 generation, Xanthine oxidase, Myeloperoxidase, Lactate dehydrogenase (LDH), Creatinine kinase cardiac specific (CK-MB) and nitrite with a significant (p<0.05) reduction in non-enzymic and enzymic antioxidants such as Reduced glutathione (GSH), Glutathione peroxidase (GPx), Glutathione-s-transferase (GST), Superoxide dismutase (SOD) and Catalase (CAT) coupled with a significantly high serum values of total cholesterol, triglycerides and low density lipoproteins (LDL) and a significant reduction in (p<0.05) high density lipoprotein (HDL) cholesterol. Overall, co-administration of Hcy with Garcinia kola at 200 mg/kg body weight showed a better cardioprotective and antiatherosclerotic effect on (Hcy)-induced cardiotoxicity and atherosclerosis than Kolaviron in this study.Keywords
Homocysteine (HCY), Garcinia kola, Kolaviron, Anti-Atherosclerosis, ECG Changes.References
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