Zinc, Copper, Iron, and Selenium Levels in Brain and Liver of Mice Exposed to Acrylonitrile

Abstract

The mechanism of toxicity of acrylonitrile (AN) has not been fully defined. The research described herein was undertaken to investigate the possible effects of AN on the levels of metallic elements in liver and brain of mice. Thirty-two mice were randomly assigned to four separate groups and treated intraperitoneal (i.p.) once daily for 1 week. Mice in the control group received normal saline, and mice in the three exposure groups received 5, 10, or 20 mg AN/kg b.w. Samples of brain and liver were collected immediately after decapitation. Tissue levels of trace elements (zinc, copper, iron) were determined with flame atomic absorption spectrophotometer or double channel atomic fluorescence absorption spectrophotometer (selenium). Mean brain weights of AN-treated mice were increased as a function of dose compared to controls, but there was no significant change in the ratio of liver/body weight in the four groups. While mean brain zinc decreased as a function of AN dosage, mean liver zinc of the low-dose group significantly increased (p < 0.05); mean liver copper in the medium-dose AN group was significantly higher compared to controls (p < 0.05); however, mean brain copper was increased, but the difference did not attain statistical significance in the three AN groups when compared with the controls (p > 0.05). Mean brain iron levels were significantly decreased in the middle-dose AN group (p < 0.05), but there were no consistent changes in liver iron. Tissue levels of selenium in brain and liver were similar for the control and AN treatment groups. AN induces significant and differential changes in the levels of zinc, copper, and iron in brain and liver. These changes likely play a pivotal role in mediating AN toxicity, most likely via changes in cellular redox status.

Copper handling machinery of the brain

“…The estimated copper content of human brain ranges from 2.9 to 10.7 mg Cu/g wet weight, while rat brains appear to have a lower copper content-1-2.3 mg Cu/g wet weight. 2,3 Fractionation of brain homogenates demonstrates that copper is present in all major cell compartments, with nuclei and mitochondria containing 1.12-1.3 mg Cu/g, microsomes-0.49-0.65 mg Cu/g, and the cytosol-2.56 AE 1.02 mg Cu/g. 4 Disease states alter copper concentrations in the CNS.…”

Brain–Barrier Regulation, Metal (Cu, Fe) Dyshomeostasis, and Neurodegenerative Disorders in Man and Animals

“…On account of its oxidation potential, regulation is necessary to ensure only sufficient but not excess copper is present in the brain. Copper concentrations are maintained at a constant level when maturity is achieved; in human beings this is 2.9-10.7 µg/g wet weight, whilst rat brains appear to have a lower copper content of 1-2.3 µg/g wet weight [6][7][8]. There is some ambiguity in the literature concerning the reporting of CNS copper levels at differing time points in the life cycles of individuals in health and disease, from the in utero/neonatal period (Cu increasing), maturity/adult (Cu stable), to ageing +/− dementia (Cu increase).…”

Tanshinone IIA Prevented Brain Iron Dyshomeostasis in Cerebral Ischemic Rats

“…Brain iron content was determined by Flame Atomic Absorption Spectrophotometer (Shimadzu AA-6800, Japan) [18]. Tissue samples (0.1~0.2 g) from brain cortex were digested with a mixture of HNO 3 and HClO 4 (4:1) for 10 h, then heated to boring.…”