Abstract

The intracellular distribution of copper in the liver has been investigated in dogs and humans. However, this has not been reported in cats. This study aimed to assess the intracellular copper distribution in liver specimens from cats with a range of hepatic copper concentrations. Twenty-nine frozen liver specimens from cats were included. Each liver specimen was divided into two pieces for overall copper quantification and tissue fractionation. The copper concentrations in liver specimens and liver fractions were measured by flame atomic absorption spectroscopy. Five specimens had copper concentrations < 100 μg/g dry weight, eight had copper concentrations between 100 and 180 μg/g, 14 had copper concentrations between 181 and 700 μg/g, and two had copper concentrations >700 μg/g. Only one specimen had positive copper staining. Regardless of the overall concentrations, copper was mostly found in the cytosolic fraction followed by the nuclear, large granule, and microsomal fractions. Our findings indicate that similarly to other species, intracellular copper is predominantly found in the cytosolic and nuclear fractions in cats. The distribution in cats with copper-loaded conditions, such as primary copper hepatopathy, was not assessed but warrants evaluation.

Highlights

  • Copper is an essential trace element that serves as a cofactor for several enzymes that are required for growth, development, and maintenance of living cells [1, 2]

  • The highest activity of glutamate dehydrogenase was detected in the large granule fraction followed by the nuclear fraction; no significant difference in activity of this enzyme was found between fractions (p = 0.07)

  • We determined the intracellular distribution of copper in liver specimens from cats using a differential centrifugation technique to obtain four subcellular fractions

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Summary

Introduction

Copper is an essential trace element that serves as a cofactor for several enzymes that are required for growth, development, and maintenance of living cells [1, 2]. The liver plays a major role in copper metabolism and homeostasis. Dietary copper is absorbed from the small intestines and enters hepatocytes from where it is either distributed throughout the body in protein-bound forms, or eliminated through biliary excretion if there is an excess of copper [3]. Copper homeostasis is tightly regulated since excess copper can become a potentially toxic transition metal and generate reactive oxygen species (ROS) [2].

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