In Vitro Antioxidant Properties of Methanolic Leaf Extract of Vernonia Amygdalina Del

Various methods employed in evaluating antioxidant activities of various samples gives varying results depending on the specificity of the free radical or oxidant used as a reactant. This study investigated the antioxidant /radical scavenging properties of the methanolic extract of Vernonia amygdalina (MEVA) leaves and studied the relationship between the assay methods. Antioxidant capacity of MEVA was evaluated by measuring the radical scavenging activity (RSA) of MEVA on 1,1-diphenyl-2-picrylhydrazyl radical (DPPH•), nitric oxide (NO) and hydrogen peroxide (HP), hydroxyl radical (OH•) scavenging activity (HRSA), lipid peroxidation inhibition activity (LPIA) against 2,2,-azobis(2-amidinopropane) hydrochloride (AAPH) and Trolox Equivalent Antioxidant Capacity (TEAC) of MEVA against 2,2′-azinobis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt (ABTS+) radicals as well as the reducing power (RP). Assay methods were subjected to regression analysis and their correlation coefficients calculated. Results were analysed using student‟s t-test and ANOVA. MEVA exhibited highest percentage RSA of 85.8% on HP, followed by DPPH• (29.6%), OH• (26.4%) and least on NO• (21.8%). MEVA inhibited AAPH-induced lipid peroxidation by 30.0% and ABTS-induced radical by 1489% with a marked RP of 0.242±0.01. DPPH correlated excellently with RP (r2 = 0.86), TEAC (r2 = 0.94) and HRSA (r2 = 0.89), the four having good relationship with each other, while LPIA correlated moderately with HP (r2 = 0.48 and NO (r2 = 0.34). MEVA exhibited significant free radical scavenging and antioxidant activities. The assay methods correlates very well and could therefore be employed for investigating and understanding antioxidant properties and scavenging activities of plant materials.Keywords: Antioxidants, assay methods, correlation coefficient, free radicals, radical scavenging activity, Vernonia amygdalin

Studies on the toxicological effect of nevirapine, an antiretroviral drug, on the liver, kidney and testis of male Wistar rats

We investigated the toxic effect of nevirapine (NVP; Viramune®), an antiretroviral drug, on the liver, kidney and testis of Wistar rats. Twenty-one rats were assigned into 3 groups of 7 animals each. The first group served as control, and the second and third groups received NVP at 18 and 36 mg/kg body weight, respectively. Clinical signs of toxicity were not observed in the animals. NVP at both doses did not significantly ( p &gt; 0.05) alter the body weight gain, relative weights of kidney and testis, serum protein, urea, creatinine and alkaline phosphatase levels of the animals. However, NVP2 significantly ( p &lt; 0.05) increased the relative weight of liver, level of serum total bilirubin and activities of γ-glutamyl transferase, alanine and aspartate aminotransferases. NVP administration caused a dose-dependent, significant ( p &lt; 0.05) elevation of lipid peroxidation measured as malondialdehyde (MDA) content in the liver, kidney and testis of the rats. Hepatic, renal and testicular MDA were increased by 107%, 80% and 163%, respectively, in NVP2-treated rats. Elevation in MDA was accompanied by a significant ( p &lt; 0.05) decrease in the activities of hepatic, renal and testicular superoxide dismutase and catalase. NVP2 caused 43% and 32% decrease in spermatozoa motility and live/dead sperm count, respectively, and 94% increase in total sperm abnormalities. Histopathological findings showed that NVP2 caused degeneration of seminiferous tubules in testis, and severe necrosis in liver slides. NVP induced oxidative stress with corresponding decrease in antioxidant status of the rats. The changes in sperm parameters and, elevation of liver marker enzymes suggest an interference of NVP2 with these organs. </jats:p

Endocrine disruption and oxidative stress implications of artemether–lumefantrine combination therapy in the ovary and uterus of rats

In the current study, we evaluated the endocrine disruption effect and oxidative stress implication of therapeutic dose of artemether–lumefantrine combination therapy on the ovary and uterus of rats. In this respect, female rats were divided into four groups: animals were per orally treated with tween 80 (control), artemether (4 mg kg−1 body weight), lumefantrine (24 mg kg−1 body weight) and artemether–lumefantrine (artemether, 4 mg kg−1 body weight and lumefantrine, 24 mg kg−1 body weight). We found that therapeutic doses of the drugs did not change the levels of ovarian hydrogen peroxide (H2O2) and malondialdehyde (MDA), but increased uterine levels of H2O2 and MDA and reduced ovarian and uterine levels of reduced glutathione. In addition, whilst ovarian glutathione peroxidase (GPx) activity reduced in the lumefantrine monotherapy group, uterine GPx increased in the artemether monotherapy as well as the artemether–lumefantrine groups. Furthermore, the drugs reduced ovarian and uterine glutathione- S-transferase and uterine superoxide dismutase activities. The drugs reduced oestrogen level, whereas follicle-stimulating hormone was reduced by lumefantrine and artemether–lumefantrine therapies. Additionally, artemether and lumefantrine monotherapies significantly increased prolactin and progesterone levels compared with the control ( p &lt; 0.05). The results suggest that in the absence of malarial parasite infection, the drugs induced oxidative stress in the ovary and uterus and disrupt hormonal balance in the rats. </jats:p