Arsenic-induced hepatic mitochondrial toxicity in rats and its amelioration by diallyl trisulfide

The present investigation was aimed to investigate the possible protective role of diallyl trisulfide (DATS) against arsenic (As)-induced hepatic mitochondrial toxicity in rats. Mitochondria were isolated from the liver tissue of rats from all the groups. Lipid profile, lipid peroxidation, antioxidant enzyme activities, hepatic function enzymes, mitochondrial swelling, cytochrome c oxidase activity, mitochondrial Ca⁺-ATPase and Na⁺/K⁺-ATPase activity, mitochondrial calcium content and mitochondrial enzyme activities were measured. Short-term As exposure (5?mg/kg?bw/d for 28?d) caused liver damage as evidenced by changes in activities of liver enzymes. The effects of As were coupled with enhanced reactive oxygen species generation, mitochondrial swelling, inhibition of cytochrome c oxidase, complex I-mediated electron transfer, decreased Ca²⁺-ATPase and Na⁺/K⁺-ATPase activity, a reduction in mitochondrial calcium content, changes in indices of hepatic mitochondrial oxidative stress, significant increase in mitochondrial lipid peroxidation products and alterations in mitochondrial lipid profile. Significant decreases in mitochondrial antioxidants and tricarboxylic acid cycle enzymes were also found in the liver mitochondria of As-induced hepatic mitochondrial toxicity in rats. As also increased hepatic caspase-3 activity and DNA fragmentation. All these apoptosis-related molecular changes caused by As could be alleviated by supplementation with DATS, which likely suggests a protective role against As-induced hepatotoxic changes and hepatic mitochondrial toxicity. The protective effect of DATS on the liver mitochondria was evidenced by altering all the changes induced by As. Free radical scavenging and metal chelating activities of DATS may be the mechanism, responsible for the protective action against As-induced mitochondrial damage in liver.     

Depression in pregnancy is associated with decreased glutathione peroxidase activity in fetal cord blood.

The investigation of fetal cord blood (FCB) during child delivery has created a novel topic in the field of psychiatric research. The umbilical vein receives nutrients and oxygen from the mother’s circulation and transports them to the fetal circulation. Investigating fetal cord blood during delivery is beneficial for understanding the fetal environment. Depression in pregnancy is associated with medical and emotional burdens. In this study, we aimed to investigate glutathione peroxidase (Gpx) and myeloperoxidase (MPO) activity in the FCB of depressed mothers and healthy controls. Our study included 45 depressed mothers and 59 healthy controls. The FCB samples were collected from the umbilical vein during delivery. We found that Gpx levels were significantly decreased in the FCB of depressed mothers than healthy controls, medians were 0.14 U/ml and 0.16 U/ml respectively, Z: −3.567 and p < 0.001. MPO levels were similar in both groups, medians were 1.0 U/L and 1.2 U/L respectively, Z: −1.837 and p:0.066. Depression in pregnancy may be associated with decreased antioxidant levels, and this condition may cause an oxidative load, which may lead to improper brain development. Future studies should be performed in larger samples to clarify our preliminary results.     

An Update on Treatment of Drug-Induced Liver Injury

Drug-induced liver injury (DILI) has been linked to more than 1,000 medications and remains the most common cause of acute liver failure in the United States. Here, we review the most current literature regarding treatment and make recommendations for the management of this relatively common disease. Since treatment of DILI remains largely elusive, recent studies have attempted to define new management strategies for these difficult patients. Early diagnosis and withdrawal of the suspected medication is the mainstay of treatment of DILI. For acetaminophen and Amanita mushroom poisoning, there are specific therapies in use. Finally, there are other possible management modalities for DILI, including corticosteroids and ursodeoxycholic acid.