BACKGROUND: Cadmium is a heavy metal harmful to animals and humans. Exposure to it causes inflammation, apoptosis, or necrosis in numerous tissues, including the adrenal.OBJECTIVES: The present research investigates the effect of cadmium toxicity on the expression of genes involved in inflammation and fibrosis. Inflammation increases the rate of parenchymal cell death, and fibrosis will only fill the place of dead cells without being able to perform the function of the primary parenchyma.METHODS: In this research, cadmium chloride with a concentration of 20 mg/kg was added to the diet of ten mice in two groups of five. On the 30th day of the study, the adrenal glands were quickly sent to the laboratory. The expression of NF-kB/MAPK, hematoxylin, eosin tissue staining, and immunohistochemistry (CD163) were performed.RESULTS: The inflammation mentioned in others’ research can also be associated with the activation of the nuclear factor kappa (NF-kB) pathway. NF-κB gene products initiate mitogen-activated protein kinase (MAPK) and p38 pathways. Previous studies indicate that MAPK induces necrosis or apoptosis in tissues. In histopathology, dense and possibly pyknosis nuclei are more common in the cadmium group. The higher expression of the CD163 molecule in the cadmium group reveals the beginning of the fibrosis process after chronic inflammation.CONCLUSIONS: This report provides more basic data to investigate the mechanism of adrenal damage in cadmium poisoning. Cadmium causes the death of cells by affecting the inflammatory pathways. Additionally, the stimulation of the fibrosis process causes greater irreparable damage to the damaged tissue of the adrenal gland.

Cadmium (Cd), a prevalent heavy metal pollutant, is known for its harmful effects on physiological functions within the biological system. In this study, the effects of Cd exposure on some kidney related biochemical and histopathological parameters in rabbits were investigated, alongside exploring the potential protective role of methanolic extract from Phoenix dactylifera (MEPD) on the kidney. The study included 45 male rabbits, aged 24-28 weeks and weighing approximately 1.41-1.43 kg were assigned into five (5) treatment groups (control, Cd-only, Cd + 300 mg MEPD, Cd + 600 mg MEPD and Cd + 900 mg MEPD) in a completely randomized design. The rabbits received a 7-day dose of 3 mg CdCl2/kg feed, followed by MEPD every 72 hours for 28 days. Results revealed higher significant (P<0.05) differences in serum glucose, urea and creatinine in Cd-only treated group when compared with the control group. MEPD treatment significantly (P<0.05) lowered serum glucose levels in Cd-exposed rabbits, indicating a potential glycemic modulating activity, but had no significant (P>0.05) effect on urea and creatinine concentrations. High density lipoprotein (HDL), low-density lipoprotein (LDL) and cholesterol ratios were not significantly different but showed marginal improvement in the Cd+MEPD groups compared to the Cd-only group. The findings also revealed significant differences in both absolute and relative kidney weights between the group treated with Cd alone and the control group, indicating potential renal injury induced by Cd. Histopathological examination revealed kidney damage in Cd-exposed rabbits, with observed changes such as disruption of Bowman’s capsule, glomerular shrinkage, degeneration of renal tubules and haemorrhage. The administration of MEPD did not ameliorate the observed histopathological alterations. In conclusion, this study suggests that Cd exposure may induce hyperglycemia and kidney injury in rabbits. MEPD treatment demonstrated some protective effects against Cd-induced hyperglycemia but did not significantly mitigate kidney damage.

Present study was carried to evaluate the toxicity of the Pb and Cd elements on the larvae of Culexquinquefasciatus. In the laboratory 5 concentrations of lead nitrate and cadmium nitrate , namely 10, 20, 30, 40, and 50 mg\l and 1, 1.5, 2, 2.5, and 3 mg\l of Pb and Cd respectively in each concentration 10 larvae were introduce beside there was a control (0mg/l). Statically analysis results declare that 1st and 2nd instars effected significantly in comparison with the control .Mortality percentage reached 28, 38.7, 48, 58, and 73.5 % in concentration 10, 20, 30, 40, and 50 mg\l respectively of lead nitrate. On the other hand, cadmium nitrate mortality percentage reached 44, 55, 65, 74.5, and 79.5 % in concentration 1, 1.5, 2, 2.5, and 3 mg\l respectively. Also, LC50 was going higher as the larva going older, measured 14.7, 16.9 for 1st and 2ndinstars and 22.3 and 41.4 for 3rd and 4th instars. On the other hand, cadmium nitrate appeared more effect than Leadnitrate with LC50  of 0.9, 1.05, 1.3, and 1.8 mg\l for 1st, 2nd, 3rd, and 4th instars respectively.

This study was conducted to evaluate the antioxidant activity of ginger (zingiber officinale) in preventing oxidative stress ,lipid peroxidation and changes in trace elements induced by cadmium toxicity in male rabbits . For this purpose twenty four of adult male rabbits were divided randomly in to four groups ( 6 in each). Group 1 was given distilled water and considered as control group, group 2 received ( 10mg/kg B.w) of cadmium chloride , group 3 received ( 100mg/ kg B.w) of ginger extract plus (10mg/kg B.w) of cadmium chloride , group 4 received (200mg/ kg B.w) of ginger extract plus of cadmium chloride(10mg/kg B.w) . All treatments were orally given a single dose for 35 days. The water and food were provided add libitum. After the end of the treatment blood samples were taken for biochemical analysis to estimate serum Malondialdehyde ( MDA) , Antioxidant activity (Glutathione , Superoxide dismutase and Catalase ) and Trace elements (Zinc, Copper and Iron ) . The result showed that the administration of cadmium chloride resulted in a high concentration of malondialdehyde ( MDA) and caused a significant decrease in both superoxide dismutase and catalase and reduced glutathione. Serum levels of trace elements were also significantly decreased. While , ginger extract administration and cadmium chloride increased and restored their levels to near normal in comparing with cadmium chloride treated rabbits.

The analytical method of trace toxic metals in livestock products was confirmed and validated through certified reference material (CRM) and the international proficiency tests. There are some difficulties to determine low levels of toxic metals in livestock products because of interferences due to the matrix. The recoveries of CRM (NIST 1577c) ranged from 73.9 to 119% for lead and from 86.4 to 111% for cadmium in bovine liver. The international proficiency tests were carried out with the milk powder and cocoa powder samples including metals provided by Food Analysis Performance Assessment Scheme (FAPAS∨®, UK). The test samples were prepared by microwave digestion using solution of HNO₃: H₂O₂ : H₂O (v/v/v = 5 : 2 : 4) and analyzed by ICP/MS. The analytical result of cadmium in milk powder was 121 ㎍/kg with .0.3 of the z-score compared to the assigned value of 131 ㎍/kg by FAPAS∨®. The analytical results of lead and cadmium in cocoa powder were 29.2 ㎍/kg and 97.6 ㎍/kg, respectively, which satisfied the assigned values of 34.2 ㎍/kg for lead and 126 ㎍/kg for cadmium by FAPAS∨®. It is verified that the analytical method is accurate and reliable to determine trace lead and cadmium in livestock products by microwave digestion and ICP/MS.