These results suggest that the higher liver core microsomal membrane fluidity observed in SHR might be dependent on the increased proportion of mono-unsaturated fatty acids. Such observed modifications and the alterations in delta9 and n-6 delta6 desaturase activities suggest that an impaired polyunsaturated fatty acid biosynthesis is related to changes in microsomal membrane fluidity in hypertension.

Vanadium may or may not be a cholesterol-lowering agent. It could potentially be used as an additional therapy or alone in therapies for treatment of dyslipidemia. This study aimed to investigate the effect of vanadium on hypercholesterolemia in the presence and absence of statins. Sixty rats were divided into five groups. The first group was kept on a normal diet and the second group was kept on a high fat diet. The three remaining groups of rats were prepared for the treatment; one group received simvastatin, one was given vanadium, and the third group was tested with both. Blood samples from all groups were investigated. Body functions were considered a tool in expressing efficacy and toxicity for the three types of treatment and were compared with the control groups. Vanadium alone causes marked increases in cholesterol levels. When added to statins, all lipid values were negatively affected as compared to the statins-only treated group. Rats with high fat diets showed significant (P≤ 0.05) elevation in the levels of serum triglycerides (TG), total cholesterol (TC), low density lipoprotein concentration (LDL-C) and very low density lipoprotein concentration (VLDL-C) as compared to the control group. All generated data proved that vanadium is impracticable for treating dyslipidemia. Vanadium is not safe or efficient in therapies for lowering cholesterol and other lipid levels.