Abstract
Boric acid (BA) is used as an antioxidant and anti-inflammatory agent, and for regulating mitochondrial membrane potential in many disorders. We investigated the protective effects of BA against chronic ethanol toxicity in rat kidney. We used 32 male rats in four groups of eight: control (C), BA, ethanol (E), and ethanol + BA (E + BA). Kidney samples were taken for histology and biochemistry. Kidney injury was assessed using hematoxylin and eosin (H & E) and periodic acid-Schiff (PAS) staining. TUNEL and caspase-3 immunohistochemistry were used as indicators of apoptosis. We measured biochemical markers of ethanol induced oxidative stress in the kidneys including malondialdehyde (MDA), total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI). The E + BA group TOS, OSI and MDA levels decreased, whereas the TAS level increased compared to group E. Caspase-3 and TUNEL activity in the E + BA group were decreased compared to group E. BA acted as an antioxidant against renal tubule injury caused by chronic use of ethanol. BA protects against apoptosis in renal tubules by decreasing oxidative damage.
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