FEMALE RATS EXPOSED TO MANGANESE CHLORIDE

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.