Objective: The purpose of this work is to examine the protective effect of nanocurcumin and nanochitosan supplementation against potassium dichromate toxicity in male mice. Methods: Male albino mice weighing 25-30 gm were divided into six groups; the first group received saline. Second and third groups were given oral dose of nanocurcumin and nanochitosan respectively for 5 d. Fourth group was injected subcutaneously with a single dose of potassium dichromate for 24 h. Group five and six were administrated nanocurcumin and nanochitosan, respectively prior to potassium dichromate. Animals were anesthetized by ether anesthesia then bone marrow was harvested for chromosomal examination and epididymal sperms were collected for sperm morphology, while Kidneys and testes were collected for western blot and biochemical analysis. Results: Potassium dichromate induced significant (P≤0.05) increase in chromosome and sperm abnormalities as well as testicular and renal MDA, renal MPO, renal contents of IL-18 and IGF-1, testicular contents of caspase 3 and cytosolic cytochrome c, a reduction in testosterone level, and GPx of renal and testicular tissues compared to control group. Pretreatment with both types of nanoparticles showed significant (P≤0.05) mitigation against most alterations induced by potassium dichromate; moreover, nanochitosan gave more significant (P≤0.05) improvement against chromosome and sperm abnormalities than nanocurcumin. Conclusion: The present study revealed that the selected nanoparticles have antioxidant as well as antigenotoxic properties against toxicity of potassium dichromate.

Objective: The aim of the present investigation was to study the potential effect of sweet orange juice against liver genotoxicity induced by lannate. Methods: adult 36 female rats were divided into 6 groups: group C (control group), group L (lannate group) injected intraperitoneal (i. p.) with 1 mg/kg b. wt. lannate for one day, group J (orange juice group) orally administered a dose of 0.1 ml/10 g b. wt. of orange juice for 48 h, group J+L received the orange juice prior to lannate, group J with L received lannate in continuous with the orange juice and group L+J received lannate prior to the orange juice. Tested parameters were DNA fragmentation, micronucleus, histopathology examination and biochemical analysis. Results: it was found that, the intake of lannate caused high DNA fragmentation and significant increase (P<0.001) in the number of micronucleated polychromatic erythrocytes in the bone marrow. Furthermore, lannate exhibited some pathological changes in the liver tissues as well as a significant (P<0.001) decrease in the total antioxidative capacity (TAC) and a significant increase in the total oxidative capacity (TOC). On the other hand, orange juice administration of all treatments (pre-treatment, continuous and post-treatment) gave some amelioration against liver damage induced by lannate. While the best results were evidenced in the continuous treatment group where the juice could attenuate liver DNA fragmentation and significantly decreased (P<0.001) the number of micronucleated polychromatic erythrocytes. In addition, it improved the induced degenerative histopathological changes as well as ameliorated the changes occurred in TAC and TOC significantly (P<0.001). Conclusion: the antigenotoxic impact of orange juice against lannate was therapeutic and hence can counteract the poisonous effect of the pesticide in people who exposed to it.