The present study was conducted to evaluate the toxic potential of tartrazine, a food color, in different tissues in adult rat: blood, liver, kidneys, and spleen. Tartrazine was administered orally at a dose of 300 mg/kg of body weight to adult male Wistar rats during a period of 30 days. Tartrazine treatment led to an increase in platelets count, a reduction in peripheral lymphocytes and in spleen T CD8-lymphocytes. Furthermore, tartrazine increased the activities of hepatocellular enzymes and promoted changes in kidney biomarkers. In order to explore the possible mechanism involved, oxidative-stress assessment was performed. Results identified critical oxidative alterations in all tested organs, as shown by the promotion of lipid peroxidation and the modification of endogenous antioxidant-defense enzymes. Thus, tartrazine is able to induce in adult rats’ hematotoxicity, immunotoxicity, and liver and kidney injuries by changing the whole balance between oxidants and antioxidants.

Abstract. Carbosulfan (CB)-induced oxidative stress leads to the inevitable accumulation of free radicals and eventual alteration of antioxidant enzymes in various biological systems. The present study is designed to investigate the preventive effect of N-acetylcysteine (NAC) on carbosulfaninduced hepatic and renal dysfunction in rats. Rats exposed to CB and NAC were examined for toxicity by assessing various biochemical alteration and stress markers including in liver and kidney. Significant increases of blood alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma glutamyltransferase (GGT), creatinine and urea were detected in CB-treated rats. In addition, the levels of antioxidative enzymes such as catalase (CAT), superoxide dismutase (SOD) and reduced glutathione (GSH) also were assessed. According to the results, rats exposed to carbosulfan showed a significant increase in the accumulation of stress markers and an alteration in the antioxidative enzymes activity, when compared to their respective controls. Interestingly, administration of NAC to CB-treated rats attenuates the toxicity of this compound, objectified by biochemical and oxidative improvement of liver and kidney. Thus, the present study reports for the first time that NAC could be a promising therapeutic agent against CB-induced oxidative stress.

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The present study investigated the protective effects of N-acetylcysteine (NAC), is widely known as an antidote to acetaminophen overdose, on carbosulfan (CB)-induced hematotoxicity and oxidative stress in male rats. CB was administered at a dose of 25 mg/kg or simultaneously administered with NAC (2 g/l) for 30 days. Results of hematological examination showed that red blood cells, hematocrite, hemoglobin, and reticulocytes levels were significantly lower in CB-exposed rats compared with those in the control. Administration of CB caused a significant increase in the superoxide dismutase and catalase activities. However, the glutathione (GSH) and thiols group (TSH) levels were significantly increased as well as GSH S-transferase activity and levels of glutathione peroxidase on erythrocytes of males rats compared with those in the control. Also, CB-treated rats showed significant elevation in lipid peroxidation (LPO) and acetylcholinesterase (AChE) on erythrocytes in comparison with the control. Co-administration with NAC exhibited chemoprotective effects against CB-mediated hematotoxicity, augmented erythrocyte antioxidant status, and prevented the induction of anemia.