Abstract

Dyslipidaemia is characterised by enhanced production of reactive oxygen species and increased oxidative stress, which may affect liver, kidney and heart function. It is considered as a critical risk factor for cardiovascular and liver diseases. The aim of our study was to assess the effect of vanadium chloride on the oxidative stress state of liver, kidney and heart functions along with electrolyte balance during treatment of dyslipidemia using simvastatin in an animal model.  Rats were assigned to 1 of 5 groups: group 1, control group; group 2, received high fat diet (HFD); group 3, received HFD and 30 mg/kg body weight (BW) simvastatin; group 4, received HFD and 15 mg/kg BW vanadium chloride and group 5, received HFD, simvastatin and vanadium chloride. Drugs were administered orally by gavage for the last week of the experimental period. HFD was found to elicit a significant decrease (P ≤ 0.05) in non-protein sulfhydryls and significant increases (P ≤ 0.05) in hepatic and cardiac malondialdehyde (MDA), serum creatine kinase, lactate dehydrogenase, creatinine, urea, uric acid, calcium, sodium and potassium. Oral administration of vanadium chloride did not synergize simvastatin to ameliorate the negative effects of HFD, instead it worsens the negative effect of the HFD. Vanadium chloride administration decreased the concentration of non-protein sulfhydryls and increased MDA concentration in liver and heart tissues. It also caused further increase in the serum concentration of all measured serum parameters. These data proved that the vanadium concentration used in this study is not safe or efficient in ameliorating the oxidative stress or in improving kidney or heart functions in dyslipidemic rats.

Key words: Vanadium, simvastatin, oxidative stress, kidney, rats.