Potential protective effect of honey against paracetamol-induced hepatotoxicity

Paracetamol overdose causes severe hepatotoxicity that leads to liver failure in both humans and experimental animals. The present study investigates the protective effect of honey against paracetamol-induced hepatotoxicity in Wistar albino rats. We have used silymarin as a standard reference hepatoprotective drug. Hepatoprotective activity was assessed by measuring biochemical parameters such as the liver function enzymes, serum alanine aminotransferase [ALT] and serum aspartate aminotransferase [AST]. Equally, comparative effects of honey on oxidative stress biomarkers such as malondialdyhyde [MDA], reduced glutathione [GSH] and glutathione peroxidase [GPx] were also evaluated in the rat liver homogenates. We estimated the effect of honey on serum levels and hepatic content of interleukin-1beta [IL-1beta] because the initial event in paracetamol-induced hepatotoxicity has been shown to be a toxic-metabolic injury that leads to hepatocyte death, activation of the innate immune response and upregulation of inflammatory cytokines. Paracetamol caused marked liver damage as noted by significant increased activities of serum AST and ALT as well as the level of II-1beta. Paracetamol also resulted in a significant decrease in liver GSH content and GPx activity which paralleled an increase in II-1beta and MDA levels. Pretreatment with honey and silymarin prior to the administration of paracetamol significantly prevented the increase in the serum levels of hepatic enzyme markers, and reduced both oxidative stress and inflammatory cytokines. Histopathological evaluation of the livers also revealed that honey reduced the incidence of paracetamol-induced liver lesions. Honey can be used as an effective hepatoprotective agent against paracetamol-induced liver damage

Caffeine induced fetal neural tube defects in mice and its influence on valproate teratogenesis

The effect of caffeine on fetal neural tube development was investigated in mice. Various oral dose regimens of caffeine were administered on gestation day-8 [GD8], GD9 or both to pregnant NMRI mice and fetuses were then examined on GDl8. Administration of caffeine [50 and 100 mg/kg] once daily on GD8 and on GD9 produced a dose-related increase in the incidence of spina bifida occulta [8.1% and 13.9%, respectively]. Administration of caffeine [50 mg/kg] three times 6 h apart on GD9 produced a higher incidence of spina bifida occulta reaching 27%. Fetuses with exencephaly were not observed as a result of administration of caffeine using either dose regimens [except of an odd fetus in the low dose group of the first regimen] or when caffeine [100 mg/kg] was given as a single administration on GD8. The influence of caffeine on sodium valproate [VPA]-induced neural tube defects [NTDs] was also studied. The study concluded that oral administration of caffeine [50 and 100 mg/kg] once daily on GD8 and on GD9 induced fetal spina bifida occulta in mice but the incidence was higher when the drug was given at the low dose three times on GD9. Furthermore, caffeine did not seem to influence VPA-induced NTDs when given either on GD8 or on GD9

Toxic effects of N-hexane on the brain, lungs, liver and testis of the exposed rats

N-Hexane is an important volatile solvent. It has been used in many industries and occupational toxic exposure was reported by many authors as Buitatti, et al. [1978] and Bragnone, et al. [1980] among the vinyl sandal and leather workers. This study were performed on albino rats. N-Hexane was given by intraperitoneal injection in the following order: 75, 150, 300 mg/kg body weight twice a week for three exposed groups I, II, III, respectively. A control non-treated group was injected with 1% tween 80 in the same order. The toxic effects were noticed on brain, liver, lungs and testicles of the treated groups. The brains of the exposed rats did not show any significant change in the oxygen uptake compared with the control group. However, they showed marked histopathological changes. There was significant decrease in the oxygen uptake by the liver of exposed groups I, II, III [70.23, 34.84, 3.67 ml / 100 g wet tissue, respectively] in comparison to that of the controls [119 ml / 100 g wet tissue], together with a dose related increase in the liver function enzymes. Lungs showed a toxic response in the form of emphysematous changes, bronchiolar hyperplasia and peribronchiolar lymphocytic infiltration. The n-hexane effect on the testis was observed in the form of decrease in the average diameter of the semineferous tubules 310, 260 and 240 micrometers in groups I, II, III, respectively, in comparison to the control group [420 micrometer]. This study indicates a definite toxic effect of n-hexane on the brain, lung, liver and testis of the exposed rats