In this study, the effects of a potent antioxidant, selenium, on apoptosis induced by acrolein, a cytotoxic and genotoxic environmental pollutant, were investigated by immunohistochemical and electron microscopic methods. One hundred adult male Wistar albino rats were used in the study. The rats were divided into four main groups: control, acrolein, selenium, and acrolein + selenium. The animals in the experimental groups were given 1 mg/kg/day selenium and 4 mg/kg/day acrolein daily for 7 days by gavage. After drug administration, each group was divided into subgroups according to the time they were to be euthanized: 12th hour, 1st, 2nd, 3rd, and 5th day. The rats in each group at the determined time were euthanized and their livers were removed. Routine histological procedures were performed for light and electron microscopy examinations. After applying the Terminal Deoxynucleotidyl Transferase dUTP nick end labeling assay on the liver sections, apoptotic index values were calculated. Comparing the liver sections of the rats in the acrolein group and the control group, acrolein was found to cause a significant increase in the apoptotic index. The apoptotic index values of the acrolein + selenium group decreased compared to the acrolein group. In the electron microscopic examinations, apoptotic findings were observed in the liver tissues of the rats given acrolein, such as chromatin condensation in the nucleus of hepatocytes, dilatations in the perinuclear space, and cytoplasmic vacuolization. These apoptotic findings were not observed in the acrolein + selenium group after the 12th hour. These findings show that selenium may potentially be useful as a protective agent for people exposed to acrolein.
Rosiglitazone is in the thiazolidinedione class of drugs used in the treatment of type 2 diabetes mellitus. It works as an insulin sensitizer by binding to the peroxisome proliferator-activated receptor gamma. We investigated the effects of prenatally administered rosiglitazone on pyramidal cell numbers and morphologies in the hippocampus at postnatal period using histochemical and stereological techniques, congenital morphological properties and the number of offspring in rats. Eighteen female rats were grouped into control (C), low-dose rosiglitazone (LDR) and high-dose rosiglitazone (HDR). LDR pregnant rats received 2 mg/kg/day of rosiglitazone via oral gavage during the first 16 days of the pregnancy. HDR rats received 5 mg/kg/day. The infants were grouped into newborn (NB), 4 week (4 W) and 12 week (12 W). A side from histopathologic and congenital assessments, stereological analyses were performed using the optical fractionator method. Congenital anomaly was not detected in any of the rosiglitazone treatment groups, and their number of offspring was similar to that of the C group. Stereological counts revealed a significant reduction in the number of hippocampal pyramidal cells in the C and LDR groups but not in the HDR group until birth to 12th week. When NB groups were compared, the number of pyramidal cells in the HDRNB group was less than those in the LDRNB and CNB groups. HDR affected apoptosis or the proliferation and maturation of progenitor cells to the pyramidal neuron during neurodevelopment in the hippocampus, whereas LDR did not adversely affect neuronal development and did not cause congenital anomalies.
Objective: Aluminium (Al) is quite abundant in nature and humans are frequently exposed to Al in daily life. Aluminium salts can exist in different forms and they may have toxic impacts on several tissues including brain. In this study, potential preventive effects of amino-guanidine (AG) (100 mg/kg, i.p.), an inducible nitric oxide synthase inhibitor, on neuron damage to be created by aluminium sulphate (3 mg/kg, i.c.v.) in cerebellar Purkinje cells were determined. Methods: 24 female Wistar albino rats were divided into 4 groups with 6 rats in each: Control (C), Sham (S), Aluminium sulphate (Al2(SO4)3), Aluminium sulphate + Amino-guanidine (Al2(SO4)3+AG). A single aluminium sulphate (3 mg/kg) dose dissolved in 0.9% NaCl was injected intracerebroventricularly to aluminium sulphate and aluminium sulphate + amino-guanidine groups at the beginning of experiments. Following aluminium sulphate injection, amino-guanidine (100 mg/kg) dissolved in distilled water was injected to aluminium sulphate + amino-guanidine group intraperiteonally for 15 days. Nothing was administered to control group, a single dose of 0.9% (3 mg/kg, i.c.v.) sodium chloride (NaCl) was administered to sham group at the beginning of experiments. Cerebellum tissues of the rats were removed 15 days after treatments and they were assessed histopathologically and stereologically. Results: Stereological optic fractionation method revealed cerebellar total number of Purkinje cells as 417615±16238,8 in control group; 378650±20171,6 in Sham group; 272945±15499,5 in Aluminium sulphate group; 324581±16324,8 in Aluminium sulphate + Amino-guanidine group.
Conclusion:It was concluded based on present findings that amino-guanidine reduced aluminium induced Purkinje cell loss through nitric oxide synthase (NOS) inhibition.
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