In addition, sinusoidal dilatation and extensive hepatic necrosis were also found. The liver necrosis probably led to the death of mice. The great doses lead to the declining liver function, since the liver had to work hard. Urine excretion of toxic compounds through from the liver is one of the essential route of elimination. Therefore, many mechanisms underlie the renal toxicity. Mild irritation or effect of a lesion (scratch) because of foreign components in high concentration might also lead to high risk of tubular necrosis.

The figure indicates a mild degeneration, namely, congestion in the kidney of the mice in control group after the dosing of extract. The congestion could selleck kinase inhibitor probably be attributed to the daily dosing of extract and the effect of solvent chemical substance given to the mice that led to mild toxicity in the kidney of mice in control group. Mice in the group treated with 5000 mg/kg had tubular necrosis. Necrosis is a sign of serious damage in the liver, which eventually

led to the death of mice. In addition, an accumulation of protein was found in the tubules. This confirms the serious renal damage. As a result, protein could not be filtered well and left in the tubules, leading to proteinuria in the mice. Serious damage in the kidney might be attributable to daily exposure of high-dose extract that lead to overwork selleck chemicals in the kidney. Finally, the kidney could not function PAK6 well. This describes the toxicity in the kidney of mice. In conclusion, crude extracts of Neopetrosia exigua caused strong activities against P. berghei indicating that extract of Neopetrosia exigua contain some lead antiplasmodial compounds. It would be worthwhile to isolate its active constituents and characterize their exact mode of action which can be exploited for the treatment of malaria. All authors have none to declare. The research was funded by Endowment B, Project Id : 12-396-0874. IIUM is gratefully acknowledged. “
“Co-amoxiclav (Fig. 1) is one of the potent broad spectrum antibiotics in the market today. It is made up of amoxicillin1 and 2

with beta-lactamase inhibitor clavulanic acid.3 It targets both Gram-positive and Gram-negative organisms especially those who have developed resistance to beta-lactam antibiotics. Co-amoxiclav’s major component is amoxicillin, which is the 4-hydroxy analog of ampicillin. It acts on the bacterial cell walls by making them more porous. Despite its wide range of germicidal action, organisms produce the enzyme beta-lactamase. Beta-lactamase protects the bacteria from being attacked by amoxicillin. Clavulanic acid, a mild antibacterial agent, helps amoxicillin by competing and irreversibly binding to the bacterial cell wall. When this happens, the targeted bacteria cannot produce beta-lactamase and will become susceptible to amoxicillin.