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Introduction: The statin-induced effects on high density lipoprotein (HDL) are relatively small compared with those of low density lipoprotein (LDL) and, as a result, most clinical trials of statins are underpowered with respect to HDL parameters. This study experimentally investigated, the effects of statin on serum lipids, atherogenic index and examined the possibility of a relationship amongst serum concentrations of HDL-C, atherogenic index and activity of lecithin:cholesterol acyl transferase. Method: Thirty albino rats equally divided into 2 groups were used for the study. Group 1 was given 0.05mg/g of statin daily for 28 days, while group 2 served as control. HDL concentration was determined as a measure of HDL-C. Total cholesterol (TC), triglyceride (TG) and HDL-C were determined spectrophotometrically while LDL-C was calculated using the Frieldwald formula. Effect on the activity of lecithin:cholesterol acyl transferase was determined by the difference between the amount of free cholesterol converted to cholesteryl ester in the two experimental groups. Effects on body and relative organs weights were also determined. Results: The administration of statin caused a significant increase in serum concentration of HDL-C, while levels of LDL-C, triglyceride and total cholesterol were reduced. Simvastatin caused a significant reduction in the atherogenic index (TC/HDL-C; LDLC/HDL-C). The administration of statin significantly induced the activity of lecithin:cholesterol acyl transferase (LCAT) as evident by reduced serum concentration of free cholesterol when compared with control. The administration of statin caused reduced body and relative organs weights. Conclusion: The study showed that serum antihyperlipidemic and antiatherogenic activity of statin may involve the induction of LCAT.
 Exposure to environmental pollutants often leads to an upsurge in the production of reactive oxygen species (ROS). ROS oxidize cellular fatty acids to produce lipid peroxyl radicals, subsequently transformed into lipid peroxides, which decrease membrane fluidity and increase the activity of various enzymes implicated in degenerative diseases and cancer formation. Edible plants that contain exogenous compounds like curcumeroid, β-carotene, turmeric, and so on, protect the aerobic cells from oxidation of free radicals. This study thus evaluates antioxidant and antimutagenic activities of ethyl acetate, aqueous and methanolic fractions of Holarrhena floribunda leaves. Inhibitory activities of the ethyl acetate fraction on Fe2+-induced lipid peroxidation in hen egg yolk; rat liver and brain tissues were also evaluated. The Allium cepa root assay was used to evaluate antimutagenic activity. Results showed that the ethyl acetate scavenged DPPH, OH•, and •O2- much stronger than other fractions, as evidenced by its lowest respective IC50 values. All the fractions displayed antimutagenic activities against cyclophosphamide-induced chromosomal aberrations. Likewise, all the fractions induced a reduction in mitotic index, a hallmark of cytotoxicity in the root meristem of Allium cepa. The decrease in mitotic index was most profound for the ethyl acetate fraction, which also demonstrated a significant lipid peroxidation inhibitory activity in the liver and brain homogenates, but not in egg yolk, compared with the ascorbic acid standard. In general, the results suggest that the ethyl acetate fraction might contain beneficial phytochemicals that should be explored as novel candidates for preclinical drug development.
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