Exploring the trichloroacetic acid-induced toxicity on the hepato-renal system and intervention by virgin coconut oil-rich diet

Abstract

Virgin coconut oil (VCO) is known for many beneficial health effects associated with its phenolic acids and flavonoid contents. We investigated the mechanisms underlying the antioxidative, anti-inflammatory, and anti-apoptotic mechanisms of Virgin Coconut oil-rich diet in treating trichloroacetic acid (TCA)-induced hepatic and renal damage in rats. Rats received TCA (250 mg/Kg b.wt, p.o) for ten days, followed by 5%, 10% or 15% VCO per gram feed for twenty-one days. Serum liver enzymes, urea, creatinine, tissue oxidative stress parameters, and inflammatory and apoptotic markers were then evaluated along with histological examination. TCA raised serum transaminases (ALT, AST), alkaline phosphatase (ALP), total bilirubin, urea and creatinine levels, which were abrogated by a VCO-rich diet dose-dependently. The activity of superoxide dismutase, catalase, glutathione peroxidase and nuclear factor erythroid 2-related factor 2 in the liver and kidney were enhanced, while malondialdehyde, tumour necrosis factor-α, interleukin-1β, nuclear factor-kB level hitherto increased by TCA were quashed by the VCO- rich diet (p<0.05). Similarly, the augmented level of Caspase-3 in the organs exposed to TCA was downregulated in favour of significantly increased BCl-2. Further, histomorphometry data validated the biochemical findings observed for the anti-inflammatory and anti-apoptotic potentials of VCO. Hepatocyte ballooning, pleomorphism and vascular congestion in the liver, loss of tubular architecture, tubular congestion and leukocyte infiltration in the kidney, all occasioned by TCA-intoxication, were evidently mitigated. Virgin coconut oil-rich diet could ameliorate liver and renal injury associated with trichloroacetic acid exposure via antioxidative, anti-inflammatory and anti-apoptotic mechanisms.