Cobalt chloride toxicity elicited hypertension and cardiac complication via induction of oxidative stress and upregulation of COX-2/Bax signaling pathway.

Cobalt is a ferromagnetic metal with extensive industrial and biological applications. To assess the toxic effects of, and mechanisms involved in cobalt chloride (CoCl2)-induced cardio-renal dysfunctions. Male Wistar rats were exposed orally, daily through drinking water to 0 ppm (control), 150 ppm, 300 ppm, and 600 ppm of CoCl2, respectively. Following exposure, results revealed significant ( p < 0.05) rise in markers of oxidative stress, but decreased activities of catalase, glutathione peroxidase, glutathione-S-transferase, and reduced glutathione content in cardiac and renal tissues. There were significant increases in systolic, diastolic, and mean arterial blood pressure at the 300- and 600-ppm level of CoCl2-exposed rats relative to the control. Prolongation of QT and QTc intervals was observed in CoCl2 alone treated rats. Also, there were significant increases in the heart rates, and reduction in P wave, and PR duration of rats administered CoCl2. Histopathology of the kidney revealed peritubular and periglomerular inflammation, focal glomerular necrosis following CoCl2 exposure. Further, cyclooxygenase-2 and B-cell associated protein X expressions were upregulated in the cardiac and renal tissues of CoCl2-exposed rats relative to the control. Combining all, results from this study implicated oxidative stress, inflammation, and apoptosis as pathologic mechanisms in CoCl2-induced hypertension and cardiovascular complications of rats.

Electrocardiographic and Blood Pressure Measurements in Captive African Lions (Panthera leo) Immobilized with Xylazine-Ketamine Combination.

Electrocardiographic and blood pressure measurements are extremely valuable diagnostic tools in the evaluationof the cardiovascular system of living animals. In this study, 6-lead electrocardiograms were recorded from five male captiveAfrican lions (Panthera leo). Also, blood pressure measurements were recorded and compared from three different sites;fore limb, hind limb and the tail, were recorded. Immobilization was done with a combination of Ketamine Hydrochloride(10mg/kg) and Xylazine (3mg/kg). Measurements were recorded as mean ± standard deviation. ECG readings were analysedusing descriptive statistics while blood pressure readings were compared using ANOVA at a 5% level of significance. Heartrate was 66±11.6 beats per minute. The heart rhythm was sinus in all the animals. Mean Electrical Axis (MEA) was between+810 and +930 degrees (Mean +89±5). Three animals had their MEA between +810 and +890 while two had MEA between+910 and +930. Fore limb measurements for Systolic Blood Pressure (SBP), Diastolic Blood Pressure (DAP) and MeanArterial Pressure (MAP) were 177.6±6.8 mmHg, 157.2±5.9 mmHg and 168.6±5.2 mmHg respectively. Hind limbmeasurements for the SBP, DBP and MAP were 135.4±9.5 mmHg, 120.6±5.9 mmHg and 123.0±6.8 mmHg respectivelywhile the tail measurements for the SBP, DBP and MAP were 149.6±8.3 mmHg, 132.8±5.9 mmHg and 137.2±5.8 mmHgrespectively. There was weak correlation between forelimb vs hindlimb and forelimb vs tail comparisons of SBP, DBP andMAP. However, a strong positive correlation was found between hindlimb and tail comparisons of those parameters. Resultsfrom this study should serve as a guide in the cardiovascular monitoring of captive African Lions immobilized with axylazine-ketamine combination.

Effect of arsenic acid withdrawal on hepatotoxicity and disruption of erythrocyte antioxidant defense system.

We investigated the effects of withdrawal from Sodium arsenite (NaAsO2) on the hepatic and antioxidant defense system in male Wistar rats using a before and after toxicant design. Rats were orally gavaged daily with varying doses of NaAsO2 for a period of 4 weeks. One half of the population was sacrificed and the remaining half had the toxicant withdrawn for another further 4 weeks. Biochemical and immunohistochemical techniques were used to assess the impact of withdrawal on the erythrocyte and hepatic systems. Exposure of Wistar rats to NaASO2 led to a significant (p < 0.05) increase in hepatic and erythrocyte markers of oxidative stress (malondialdehyde, thiol contents and hydrogen peroxide generation). Concurrently, there was a significant (p < 0.05) increase in hepatic and erythrocyte antioxidant enzymes (glutathione-S-transferase, glutathione peroxidase and superoxide dismutase) following exposure. Withdrawal from NaAsO2 exposure led to a decline in both erythrocyte and hepatic markers of oxidative stress and together with a significant improvement in antioxidant defense system. Histopathology and immunohistochemistry revealed varying degrees of recovery in hepatocyte ultrastructure alongside increased expression of the pro-survival protein Kinase B (Akt/PKB) after 4 weeks of NaAsO2 withdrawal. Conclusively, withdrawal from exposure led to a partial recovery from oxidative stress-mediated hepatotoxicity and derangements in erythrocyte antioxidant system through Akt/PKB pathway.