ABSTRACT
Griseofulvin is a well known fungicide drug. It is used to treat dermatomycosis in many species. It has toxic effects on the liver, kidney, blood and chromosomes on prolonged use. This study was conducted to evaluate the nephrotoxic effects of chronic oral administration of griseofulvin on adult albino rats. The kidneys will be investigated histopathologically by light and electron microscopes and biochemically by measuring blood urea nitrogen and serum creatinine. This study was conducted on 30 normal adult albino rats of uniform strain. The rats were divided into three groups equally, The 1[st] group was used as a negative control group, the 2[nd] [positive control group] each rat was given 1 mL of olive oil orally once dally, the 3[rd] group each rat was given griseofulvin orally dissolved in 1 mL olive oil in a dose of 2500 mg/kg body weight [1120 of LD50] daily for 12 weeks. The affected glomeruli appeared shrinked with wide Bowman's spaces and adhesion of glomeruli to their Bowman's capsules. Most of the kidney tubules appeared distorted. The mean values of blood urea nitrogen and creatinine in griseofulvin treated group showed a statistically significant increase after 12 weeks when compared with positive control group. It can be concluded that griseofulvin is nephrotoxic on chronic administration to adult albino rats
ABSTRACT
Forty type II diabetic patients [diabetic group] and 40 healthy age- and sex-matched persons [control group] were enrolled. The study involved assessment of body mass index [MBI], glycemic state [fasting and postprandial blood glucose, glycated hemoglobin [HbAlc]], low- density lipoprotein cholesterol [LDL], albuminuria by urinary albumin excretion rate [UAE], plasma PF 1+2 and TAFI, also, reverse transcriptase-polymerase chain reaction [RT-PCR] for TAFI mRNA in adipocytes and cell cultures. Plasma PF 1+2 and TAFI showed significant positive correlations with CVD risk factors including BMI, LDL and albuminuria. Also, they showed significant positive correlation with history of arterial and venous [only for TAFI] CVD. Mean values for these markers were statistically higher in the diabetic group compared to the control group. Furthermore, their values were statistically higher in patients with history of CVD compared to those without prior history. In conclusion, plasma PF 1+2 and TAFI reflected a prothrombotic and hypofibrinolysis state that may explain the increased CVD among diabetics. TAFI gene expression in adipocytes would explain the increased risk of CVD among obese diabetics