RESUMEN
Malaria is a global health problem with severe morbidity and mortality in Sub-Saharan Africa. Resistance of Plasmodium spp to the current anti-malaria drugs necessitates further search for novel effective drugs. This study, therefore, investigated the effect of sodium acetate on glucose-6-phosphate dehydrogenase in Plasmodium berghei-infected mice. Thirty male Albino mice were randomly distributed into 6 groups, A-F. Animals in Groups B-F were inoculated with P. berghei, intraperitoneally. Subsequently, Group C mice were treated with 20 mg/kg chloroquine, while groups D, E and F received 25, 50 and 100 mg/kg sodium acetate, respectively. All treatments were administered orally for 4 days. At the end of the experiment, animals were sacrificed by cervical dislocation and blood was collected via cardiac puncture for the analyses of serum glucose-6-phosphate dehydrogenase (G6PD), uric acid and lipid profile. Our results showed that Sodium acetate (50 and 100 mg/kg) significantly reduced (p < 0.05) parasitaemia (67.11% and 77.62%, respectively) than chloroquine (61.73%). Besides, body weight and serum G6PD activity in P. berghei infection were improved. Similarly, sodium acetate reduced elevated serum uric acid. Effects of sodium acetate and chloroquine on biochemical parameters were comparable (p > 0.05) but atherogenic lipid ratios were not affected by sodium acetate. These data put together suggested that activity of sodium acetate may be harnessed for development of novel anti-malaria drugs. However, more studies are required to delineate its mechanisms of action.
RESUMEN
Cardiovascular diseases are major causes of non-communicable diseases (NCDs)-related throughout the world. Water pollution has been linked with the high global NCD burden but no report exists on the cardiotoxicity of untreated or poorly treated pharmaceutical effluent, despite its indiscriminate discharge into the aquatic environment in Nigeria, as in many other locations of the world. Thus, this study investigated the cardiotoxic effect of oral exposure to pharmaceutical effluent in mice. Thirty (30) male mice (Mus musculus) were randomly divided into 6 groups. Group A (control) received 0.2 ml distilled water, while groups B-F were treated with 0.2 ml 2.5%, 5.0%, 10.0%, 20.0% and 40% concentrations (v/v, effluent/distilled water) of the effluent respectively, for 28 days. Significant reductions (p<0.05) in heart weight and cardiac weight index were observed in the groups treated with 5%, 10%, 20% and 40% concentrations of the effluent, without significant change in body weight. Similarly, 28 day administration of the effluent showed significant decrease in cardiac Na+-K+-ATPase activity (p<0.05) at concentrations 10% and above, in a concentration dependent manner. However, there was insignificant decrease in cardiac Ca2+-Mg2+-ATPase activity of the exposed mice, when compared with the control group. This study provides novel information on the cardiotoxic effects of oral exposure to untreated pharmaceutical effluent, showing reduced Na+-K+-ATPase activity and decreseased myocardial atrophy. Therefore, drinking water contaminated with pharmaceutical effluent may promote the incidence of cardiovascular diseases. Further studies on the exact mechanistic routes of the induced cardiotoxicity are recommended.
RESUMEN
Many pharmaceutical industries carelessly handle their effluents and indiscriminately release same to aquatic environment. These effluents often find their ways into surface and ground waters, contaminating public water and thus, serving as a potential threat to animals and human health. In this study, we investigated the cardiorenal effects of chronic oral exposure to pharmaceutical effluent in mice. Thirty male mice (Mus musculus) were randomly divided into groups A-F and treated with 0.2 mLs 0.0 %, 2.5 %, 5.0%, 10.0%, 20.0% and 40% concentration (v/v, effluent/distilled water) of the effluent for 28 days, respectively. At the end of the experiment, the animals were sacrificed by cervical dislocation. Activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) were determined in serum and heart homogenate, while uric acid, creatinine and electrolytes (sodium, potassium, bicarbonate and chloride ions) were determined in serum only. Data were expressed as Means ± standard error of mean and values were considered significant at p < 0.05. Results showed that, oral exposure to pharmaceutical effluent reduced (p < 0.05) cardiac ALP, AST and ALT activities as well as serum ALT activity. However, serum activities of ALP, creatinine and uric acid were elevated (p < 0.05). Similarly, there was derangement of electrolytes (potassium, chloride, bicarbonate and sodium ions) in the exposed mice, compared with control. This study has demonstrated that poorly treated pharmaceutical effluent disrupted cardiac and serum enzyme activities, caused electrolytes imbalance and elevated serum uric acid level, suggesting that, drinking water contaminated with pharmaceutical effluent may impair kidney and cardiac functions. Further study, investigating the histology of the kidney and heart of the pharmaceutical effluent-exposed animals as well as mechanism(s) of cardiorenal toxicity of the effluent, should be carried out to exploit its roles in pathogenesis of cardiorenal diseases.
