Hsp70 accumulation and ultrastructural features of lung and liver induced by ethanol treatment with and without L-carnitine protection in rats.

Abstract This study examined Hsp70 accumulation and the subcellular characteristics of liver and lung when exposed to ethanol (EtOH), with and without l -carnitine protection. Female Sprague-Dawley rats, 150–200 g body weight, were randomized into four groups: Control (CON), Alcohol (ALC), l -carnitine (CAR) and Alcohol- l -carnitine (ALC-CAR). EtOH was administered per os at a dose of 4 g/kg body weight (1 ml) daily for 4 weeks. Before alcohol intake, an oral dose of 500 mg/kg body weight of l -carnitine was also administered to the ALC-CAR group. The liver and lung samples were subjected to Hsp70 Western blot and ultrastructural analysis. The Hsp70 accumulation was higher in the liver than in the lung samples. Hepatic Hsp70 accumulation was similar for all groups in contrast to lung, where the Hsp70 accumulation depends on the group studied. The ultrastructural results showed lung but not liver alterations, evidencing a stressful condition and subsequent cellular injury for lung tissue but not for liver. The ALC-CAR group showed less lung damage than the non-protected group and resembles the general appearance of the CON and CAR groups. EtOH intoxication induced differential cellular response in liver and lung in a dose and tissue dependent manner. l -carnitine seems to reduce lung EtOH-induced subcellular damage. The promotion of heat shock or stress proteins might represent one of the mechanisms involved that need to be further investigated.