Hepatic epiphany for mysterious myrrh

A statistical analysis of experimental data on laboratory animals shows that the resin of the middle-eastern tree Commiphora, better known as "myrrh" can act as a protective antioxidant against liver damage caused by organic lead compounds.

Myrrh is a rust-coloured resin obtained from several species of Commiphora and Balsamodendron tree, native to the Middle East and Ethiopia. It is perhaps best known as one of the gifts of the Magi offered to the infant Jesus, along with gold and frankincense in the Christmas story. During that time, myrrh was revered as an embalming ointment and is also an ingredient in incense.

Through the ages, myrrh has been used in a wide range of traditional remedies over the centuries as a mouthwash, for treating sore threats, bronchial congestion, as well as an antiseptic astringent, for soothing cuts and burns, and for various other less well-convincing purposes, such as calming emotions.

Khaled Ashrya, Yasser El-Sayeda, Rania Khamiss, and Ibrahim El-Ashmawy in the Faculty of Veterinary Medicine, at Alexandria University, in Behera Province, Egypt, point out that myrrh may have even wider medical applications. "A few studies have investigated the immunomodulatory effects of myrrh," they explain and other researchers have suggested that it stimulates phagocytosis in vivo. Indeed, dietary supplementation improves the cellular immune response by triggering lymphocyte transformation, phagocytic activity and boosting the phagocytic index in laboratory mice intoxicated with lead. With this in mind, the researchers hoped to discover whether an emulsion of this substance could reduce or even prevent oxidative stress caused by lead poisoning.

Lead is a cumulative and non-essential metal ion in the body with a wide range of toxic effects. "Today, it is widely accepted that even small quantities of lead are harmful to humans and animals," the researchers say, "It is implicated in a broad range of acute or chronic behavioural, biochemical and physiological conditions." Despite its importance as a toxic pollutant, little is known about the detailed biochemical mechanisms involved in lead's toxic impact on the liver. However, it is known that hepatotoxicity arises because lead's ability to generate reactive oxygen species. A 2007 paper offered conclusive evidence that lead-induced lipid peroxidation of cellular membranes in the liver plays a critical role in hepatotoxicty.

Another aspect of lead's toxicity is that it has a strong affinity for sulfhydryl groups in proteins (in other words reduced glutathione) and especially the amino acid cysteine. It has been suggested that this affinity for sulfur interferes with the antioxidant barrier provided by functional SH groups in enzymes such as glutathione reductase, glutathione peroxidase, glutathione S-transferase, superoxide dismutase, catalase and delta-aminolevulinic acid dehydratase all of which are thought to be critical to the ability of mammalian cells to protect themselves against reactive oxygen species.

The protective, antioxidant effects of alpha-tocopherol, ascorbic acid and L-methionine against lead-induced oxidative stress to the liver, kidney and brain in rats, have been demonstrated previously. This, and other evidence, suggests that protection with antioxidants might be the best course of action to avert lead poisoning.

Now, the Alexandria team has investigated the potential of a Commiphora molmol emulsion (CME) in protecting against hepatoxicity caused by lead acetate in laboratory rabbits. They tested six groups of animals: groups I (control) and II (PbAc) were given no CME. Groups III (CME50) and IV (CME50 + PbAc) were administered with CME in a dose rate of 50 milligrams per kilogram of body weight, while groups V (CME100) and VI (CME100 + PbAc) received 100 mg CME/kg daily for 14 weeks. The team gave Groups II, IV and VI 80 mg PbAc/kg each day orally for 6 weeks starting from the 9th week.

An analysis of the data showed that the PbAc-group had a 220% increase in hepatic malondialdehyde levels, while glutathione, glutathione S-transferase and glutathione peroxidase levels decreased. The team also found that lead-acetate induced problems with proteins and increased activity in aminotransferase enzymes. However, problematic biochemistry in those animals pre-treated with CME appeared to have dose-dependent protection against the adverse effects of lead acetate administration.

"CME, therefore, is a potent antioxidant, and can protect against PbAc-induced hepatic oxidative damage and immunotoxicity by reducing lipid peroxidation and enhancing the antioxidant and immune defence mechanisms," the team concludes.