Di(2-ethylhexyl) phthalate (DEHP) is ubiquitous environmental contaminant and identified as endocrine-disrupting chemical (EDC), present in plastics as plasticizer. Due to its versatile use, human exposure level reaches to danger limit. The main focus of our study is to see the effect of vitamin C on hematological and biochemical alterations caused by Di(2-ethylhexyl) Phthalate toxicity in female albino mice,
Mus musculus
. It is found to cause defects of the liver, kidney, and lungs. Its anti-androgenic nature brings the main focus on its toxicity associated with reproductive and endocrine system. In this experimental study, 18 young female Swiss albino mice,
Mus musculus
, were used and divided into 3 groups of 6 animals each as control (corn oil vehicle), DEHP group (100 mg/kg body weight dissolved in corn oil), and DEHP + vitamin-C group (100 mg/kg body weight each, dissolved in corn oil and double distilled water, respectively) for 90 days. In this research, serum metabolites were evaluated to study the effect of DEHP on glucose, total protein, and lipid profile along with some hematological, enzymological, and oxidative stress parameters. Simultaneously, we compared the effectiveness of vitamin-C against DEHP toxicity to mitigate the serum homeostasis disturbance. In present study, we observed, in DEHP-treated animals, glucose, triglycerides, very-low-density lipoprotein (VLDL), total protein, alkaline phosphatase (ALP), acid phosphatase (ACP), and alanine aminotransferase (ALT) levels increased remarkably, whereas total cholesterol, high-density lipoproteins (HDL), aspartate aminotransferase (AST), total RBC count, total WBC count, and hemoglobin (Hb) level significantly decreased as compared to control group. In addition, we noticed there was a decrease in superoxide dismutase (SOD) and increase in levels of lipid peroxidation (MDA) and interleukin-6 (IL-6) in DEHP treatment group as compared to control group. The results indicated vitamin C had a better improving effect against DEHP toxicity on balancing metabolic abnormalities and inflammation-related comorbidities.
