S.O. OLUBODUN

Manganese is a trace element and an environmental pollutant widely used in industries, but excessive exposure is associated with multi-organ toxicity. While its neurotoxic effects are well documented, its impact on metabolic and renal functions is less explored. Manganese toxicity is known to promote oxidative stress, which can disrupt lipid metabolism and damage renal tissues. Cinnamic acid (CA) is a natural phenolic compound that has potent antioxidant and anti-inflammatory properties, which may offer a promising therapeutic benefit in ameliorating manganese chloride toxicity. This study evaluated the effect of cinnamic acid (CA) on the lipid profile and kidney function of female rats exposed to Manganese Chloride. Thirty (30) adult female rats were randomly divided into six (6) groups (n=5); group 1 (normal control), group 2 (10mg/kg MnCl2), group 3 (CA low dose, 50 mg/kg), group 4 (CA high dose, 100mg/kg), group 5 (MnCl2 + 50mg/kg CA) and group 6 (MnCl2 + 100mg/kg CA). Treatment was orally administered daily for 90 days. Thereafter, the rats were sacrificed under anesthesia, and blood samples were collected for lipid profile and kidney function analysis. The results revealed that the group exposed to MnCl2 without treatment had significantly (p < 0.05) impaired renal function, indicated by elevated serum urea and creatinine levels, electrolyte imbalance when compared to the normal control group. It also induced a dyslipidemic state with increased total cholesterol, triglycerides, low density lipoprotein (LDL) and decreased high density lipoprotein (HDL) levels. Co-treatment with CA demonstrated a dose-dependent ameliorative effect, as it was observed that group 6 (MnCl2 + CA high dose) showed better protection nearly normalizing the kidney function and lipid profile markers. No significant alterations were observed in groups 3 and 4 compared to the normal control. Findings from this study suggest that CA possesses renal protective and hypolipidemic potential against MnCl2-induced toxicity in a dose dependent manner. The mechanism is likely attributed to the antioxidant activity of CA which counteracts MnCl2 induced oxidative damage.

The experiment is aimed at carrying out a toxicological study on rats given different doses of both aqueous and methanol extract of Acalypha Wilkesiana and to determine the degree of toxicity on some organs of the rats fed with both aqueous and methanol extract of Acalypha Wilkesiana. A total of seventy five male albino rats were used for the whole of the experiments. For Acute toxicity study phase one of the studies alone was carried out. For sub-acute toxicity study: The rats were placed into 4 different groups and group 1 served as the control group that was fed with pellets and water, the other groups that’s group 2 to 4 was divided into 2 sub-groups (group 2A aqueous and 2B methanol), and was given different doses of plant extracts. For 28 days, to mark the end of our sub-acute toxicological study, liver and kidney function biomarkers, electrolytes, lipid profile assays were investigated. For the acute toxicity study, it was observed that there was no visible sign of toxicity or death observed in all
the animals administered with the aqueous and methanol extract of Acalypha Wilkesiana

This research examines the effect of ethanol leaf extract of Acalypha wilkisenia on malondialdehyde (MDA) and glutathione peroxidase (GPx) levels in wistar rats with 1,2 dimethylhydrazine(DMH) induced colon tumors. Colon cancer is a leading cause of cancer related mortality ,is often characterized by elevated oxidative stress markers such as MDA and altered antioxidant enzyme activities, including GPx. Alcalypha wilkisenia, a plant commonly known for its antioxidant properties, was evaluated for its potential therapeutic effects. Wistar rats were divided into six groups: Control, DMH treated only, Xeloda, DMH plus ethanol leaf extract of Alcalypha wilkisenia . Over the experimental period, MDA and GPx levels were measured using standard biochemical assays. Results indicated that DMH significantly increased MDAlevels and decreased GPx activity, indicative of oxidative stress and impaired antioxidant defense. Conversely administration of Acalypha wilkisenia extract to DMH treated rats resulted in a significant reduction in MDA levels and restoration of GPx activity , suggesting a protective effect against colon carcinogenesis through the modulation of oxidative stress markers, highlighting its potential as a complementary therapeutic agent in colon cancer management .Further studies are needed to elucidate the underlying mechanisms and confirm these effects in clinical settings