## 3 Results and Discussion
### Histopathology Analysis  
Light microscopic examination showed a normal structure of the kidney (Figure 4a) in the controls. Glomerular atrophy, tubular necrosis and widening were evident in the kidneys of all Cd-exposed animals (Figure 4b). Simultaneous administration of SeNPs with Cd, reduced the heavy metal toxic structural changes in the kidney in dose dependent manner. The kidney morphology of the LSeNPs-Cd groups did not differ from that of  
Figure 3: (**a**). Trolox concentrations-response curve of % Inhibition of ABTS\({}^{\star}\), recorded at 734 nm. Five different standard concentrations (between 0.25 and 2 mM Trolox) were used in triplicate. (**b**).The % Inhibition of ABTS\({}^{\star+}\) from blood mice after 30 days treatments. All values were expressed as mean \(\pm\) SD for 10 mice in each group. Statistically significant difference at * \(p\) < 0.05. Groups: Control-mice received only water; Cadmium group (Cd)-mice received orally 5 mg/kg CdCl\({}_{2}\); 0.1 SeNPs + Cd (0.1 mg/kg SeNPs + 5 mg/kg CdCl\({}_{2}\)); 0.2 SeNPs + Cd (0.2 mg/kg SeNPs + 5 mg/kg CdCl\({}_{2}\)); 0.4 SeNPs + Cd (0.4 mg/kg SeNPs + 5 mg/kg CdCl\({}_{2}\)); 0.1 LSeNPs + Cd (0.1 mg/kg LSeNPs + 5 mg/kg CdCl\({}_{2}\)); 0.2 LSeNPs + Cd (0.2 mg/kg LSeNPs + 5 mg/kg CdCl\({}_{2}\)); 0.4 LSeNPs + Cd (0.4 mg/kg LSeNPs + 5 mg/kg CdCl\({}_{2}\)). the control animals, offering a complete prevention from the Cd-induced changes in renal structure at highest dose (Figure 4h). Figure 4: Histopathological sections of kidney of the experimental groups, H&E \(\times\) 200. Various degrees of histopathological changes were observed in Cd exposure groups, mainly including glomerular atrophy (arrow) and tubular damage (**b**). Co-administration of SeNPs with Cd, reduced the metal toxic histological changes in the kidney in dose dependent manner, more obvious for LSeNPs. CV-centrilobular vein. Groups: Control (**a**)-mice received only water; Cadmium group (**b**)-mice received orally 5 mg/kg CdCl2; 0.1 SeNPs + Cd (**c**) (0.1 mg/kg SeNPs + 5 mg/kg CdCl2); 0.2 SeNPs + Cd (**d**) (0.2 mg/kg SeNPs + 5 mg/kg CdCl2); 0.4 SeNPs + Cd (**e**) (0.4 mg/kg SeNPs + 5 mg/kg CdCl2); 0.1 LSeNPs + Cd (**f**) (0.1 mg/kg LesNPs + 5 mg/kg CdCl2); 0.2 LSeNPs + Cd (**g**) (0.2 mg/kg LesNPs + 5 mg/kg CdCl2); 0.4 LSeNPs + Cd (**h**) (0.4 mg/kg LesNPs + 5 mg/kg CdCl2). Several histopathological studies revealed that the toxic effects of Cd in the kidney are confined with proximal tubular cells, affected by necrosis and apoptosis and tubular degeneration [48; 49; 50]. Early tubular disease in Cd nephrotoxicity [51] and tubular proteinuria continued with glomerular damage, leading to albuminuria and a progressive impairment in glomerular filtration, are injuries induced by cadmium, causing end-stage renal failure [52]. In our experiment we noticed several histopathological renal changes, including both of tubular injuries and glomerular atrophy or swelling, which are in agreement with previous toxicological results, suggesting that exposure to Cd 5 mg/kg to mice induced morpho-functional changes and renal dysfunction. Cd is absorbed from the gastrointestinal tract into the circulation by a transporter, DMT1 (Divalent Metal Ion Transporter 1), in the duodenum [53]. Once it reaches the liver it is rapidly bound to metallothionein (MT), which is then slowly released back into circulation. The Cd-MT complex is filtered at the glomerulus and reabsorbed by the proximal tubule, being a protective response to limit toxicity from free Cd (Cd2+). Unfortunately, once the MT-producing capacity of proximal renal tubular cells is exhausted, progressive tubular cell damage occurs and the intracellular levels of Cd2+ increase [54]. Cd can also induce autoantibodies to MT, which may be toxic for tubular cells and interfere with Cd detoxification [55], while other autoantibodies target induced glomerular damage [51], and manifested by morphological changes on both tubular and glomerular cells.