The Protective Potential of Aronia melanocarpa L. Berry Extract against Cadmium-Induced Kidney Damage: A Study in an Animal Model of Human Environmental Exposure to This Toxic Element

Abstract

The impact of cadmium (Cd) on the function and structure of the kidney and the potential protective effect of an extract from Aronia melanocarpa L. berries were investigated in a rat model of low- and moderate-level environmental exposure to this heavy metal (1 and 5 mg Cd/kg feed for up to 24 months). The sensitive biomarkers of Cd-induced damage to the kidney tubules (N-acetyl-β-D-glucosaminidase (NAG), alkaline phosphatase (ALP), β2-microglobulin (β2-MG), and kidney injury molecule-1 (KIM-1) in the urine), clinically relevant early markers of glomerular damage (albumin in the urine and creatinine clearance), and other markers of the general functional status of this organ (urea, uric acid, and total protein in the serum and/or urine) and Cd concentration in the urine, were evaluated. The morphological structure of the kidney and inflammatory markers (chemerin, macrophage inflammatory protein 1 alpha (MIP1a), and Bcl2-associated X protein (Bax)) were also estimated. Low-level and moderate exposure to Cd led to damage to the function and structure of the kidney tubules and glomeruli. The co-administration of A. melanocarpa berry extract significantly protected against the injurious impact of this toxic element. In conclusion, even low-level, long-term exposure to Cd poses a risk of kidney damage, whereas an intake of Aronia berry products may effectively protect from this outcome.

Chinese Sumac (Rhus chinensis Mill.) Fruits Prevent Hyperuricemia and Uric Acid Nephropathy in Mice Fed a High-Purine Yeast Diet

“…NAG is a highly sensitive indicator of renal tubular function, predominantly found in renal tubular epithelial cells. Increased NAG in urine signifies renal tubular damage [ 38 ]. As depicted in Figure 4 , the M group exhibited considerable alterations in these indicators compared to the C group, signifying severe kidney-related functional impairment due to hyperuricemia.…”

“…Current research shows that, aside from congenital conditions, the two main causes of hyperuricemia are the overproduction of uric acid and underexcretion of uric acid. UA production and excretion are primarily regulated by XOD and renal uric acid excretion [ 38 ]. Consequently, current treatments for hyperuricemia commonly involve XOD inhibitors to curb UA production or enhance renal UA excretion for increased UA elimination.…”