Using iron precipitants to remove arsenic from water: is it safe?

Arsenic-associated health complications are reported worldwide. Arsenic is a documented toxic element in drinking water. Removing arsenic from drinking water is widely dependent on iron-based techniques. Although inorganic arsenic has long been known to be toxic to humans, little is known about the toxic effect of the interaction between arsenic and iron. We investigated the effect of arsenic plus iron on the liver of rats. We gave rats sodium arsenite, iron, or sodium arsenite plus iron. Neither the arsenic-alone nor the iron-alone treatments altered their serum aspartate or alanine transaminase levels. However, a combination of non-toxic doses of arsenite and iron synergistically increased serum aspartate and alanine transaminase levels and lipid peroxidation in liver tissue. Therefore, we hypothesize that arsenic plus iron synergistically induces hepatic damage mediated through oxidative stress in rats. Our study indicates an important public health issue: using iron precipitants to remove arsenic from water may cause oxidative hepatic damage in humans.

Effect of Cassia fistula Linn. leaf extract on diethylnitrosamine induced hepatic injury in rats.

The hepatoprotective and antioxidant effect of Cassia fistula Linn. leaf extract on liver injury induced by diethylnitrosamine (DEN) was investigated. Wistar rats weighing 200+/-10g were administered a single dose of DEN (200mg/kg b.w., i.p.) and left for 30 days. For hepatoprotective studies, ethanolic leaf extract (ELE) of C. fistula Linn. (500mg/kg b.w., p.o.) was administered daily for 30 days. AST, ALT, ALP, LDH, gamma-GT and bilirubin were estimated in serum and liver tissue. Lipid peroxidation (LPO), SOD and CAT were also estimated in liver tissue as markers of oxidative stress. DEN induced hepatotoxicity in all the treated animals were evident by elevated serum ALT, AST, ALP and bilirubin levels and a simultaneous fall in their levels in the liver tissue after 30 days. Induction of oxidative stress in the liver was evidenced by increased LPO and fall in the activities of SOD and CAT. ELE administration for 30 days prevented the DEN induced hepatic injury and oxidative stress. In conclusion, it was observed that ELE of C. fistula Linn. protects the liver against DEN induced hepatic injury in rats.

Silymarin modulates the oxidant-antioxidant imbalance during diethylnitrosamine induced oxidative stress in rats.

Oxidative stress is a common mechanism contributing to initiation and progression of hepatic damage in a variety of liver disorders. Hence, there is a great demand for the development of agents with potent antioxidant effect. The aim of the present investigation is to evaluate the efficacy of silymarin as a hepatoprotective and an antioxidant against diethylnitrosamine induced hepatocellular damage. Single intraperitoneal administration of diethylnitrosamine (200 mg/kg) to rats resulted in significantly elevated levels of serum aspartate transaminase (AST) and alanine transaminase (ALT), which is indicative of hepatocellular damage. Diethylnitrosamine induced oxidative stress was confirmed by elevated levels of lipid peroxidation and decreased levels of superoxide dismutase (SOD), catalase, glutathione peroxidase, glutathione reductase (GR) and glutathione-S-transferase (GST) in the liver tissue. The status of non-enzymic antioxidants like, vitamin-C, vitamin-E and reduced glutathione (GSH) were also found to be decreased in diethylnitrosamine administered rats. Further, the status of membrane bound ATPases was also altered indicating hepatocellular membrane damage. Posttreatment with the silymarin (50 mg/kg) orally for 30 days significantly reversed the diethylnitrosamine induced alterations in the liver tissue and offered almost complete protection. The results from the present study indicate that silymarin exhibits good hepatoprotective and antioxidant potential against diethylnitrosamine induced hepatocellular damage in rats.