Melatonin, the principal secretory product of the pineal gland, functions as a potent antioxidant and free radical scavenger. Additionally, the antiapoptotic effect of melatonin has been observed both in vivo and in vitro. The aim of this experimental study was to investigate the protective effects of melatonin against carbon tetrachloride (CCl(4))-induced apoptosis and oxidative stress in rat liver. Twenty-four male Wistar rats were divided in three equal groups. Group I was used as control. Rats in group II were injected every other day with CCl(4) (0.5A mL/kg BW) for a month, whereas rats in group III were treated every other day with the same dose of CCl(4) plus melatonin (25A mg/kg BW). At the end of the experiment, all animals were killed by decapitation and the livers were rapidly removed. Some of the liver tissue specimens were used for determination of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels. The remaining tissue specimens were processed for immunohistochemical assessment, and the percentage rates of apoptotic liver cells stained with immunoreactive Bax were determined. Chronic administration of CCl(4) significantly increased liver MDA contents, as an end product of lipid peroxidation, and also significantly decreased SOD and GSH-Px activities, emphasizing the generation of increased oxidative stress. Moreover, it caused an evident increase in apoptotic cells. Melatonin treatment significantly reduced MDA levels and elevated SOD and GSH-Px activities in rats received CCl(4) plus melatonin. Furthermore, apoptotic changes caused by CCl(4) were considerably decreased in these animals. The results of the present study indicate that melatonin treatment substantially prevents CCl(4)-induced apoptosis and oxidative damage in the liver. Thus, melatonin may serve as a drug for treating many clinical conditions that arise from inappropriate apoptosis.

Exposure to cigarette smoke causes changes in the oxidative enzyme levels in rat testis, but CAPE can reverse these harmful effects.

It was aimed to investigate the histopathological and biochemical changes in kidney tissues of rats exposed to cigarette smoke and possible protective effects of caffeic acid phenethyl ester (CAPE) on these changes. Twenty one male Wistar albino rats were divided into three equal groups. Animals in group I were used as control. Rats in group II were exposed to cigarette smoke and rats in group III were exposed to cigarette smoke and daily administration of CAPE. At the end of the 60-day experimental period, all the animals were sacrificed by decapitation. The serum samples obtained from the animals were studied for uric acid, creatinine and blood urine nitrogen (BUN) levels. Following routine histological procedures, kidney tissue specimens were examined under a light microscope. In addition, dismutase (SOD) and glutathione peroxidase (GSH-Px) enzyme activities and malondialdehyde (MDA) and nitric oxide (NO) contents were determined spectrophotometrically in tissue samples. It was found that serum uric acid and BUN levels of the rats exposed to cigarette smoke alone were elevated, although serum creatinine levels did not significantly change. Furthermore, renal SOD, GSH-Px, NO and MDA levels were significantly increased. These increases in serum BUN, and renal SOD, GSH-Px, NO and MDA levels were significantly inhibited by CAPE treatment. In light microscopic observations of tissues from rats exposed to smoke, mesangial cell proliferation in the renal corpuscles, dilatation and congestion in the peritubular capillaries and degenerative alterations in the proximal tubules were noted. There were also atrophic renal corpuscles. However, these histopathological changes were partially disappeared in the rats exposed to cigarette smoke plus CAPE. The present findings indicate that cigarette smoke causes impairment in renal structure and function, which can be prevented by CAPE administration.

No abstract

The aim of this study was to investigate the histological and biochemical changes in liver of rats exposed to cigarette smoke and effects of caffeic acid phenetyl ester (CAPE) on these changes. For this purpose, 21 male Wistar rats were divided into three groups. Animals in Group I were used as control. Rats in Group II were exposed to cigarette smoke and rats in Group III were exposed to cigarette smoke and injected daily with CAPE. At the end of the 60-days experimental period, all rats were killed by decapitation and blood samples were obtained. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin levels and hepatic superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px ), malondialdehyde (MDA) contents were determined. Following routine histological procedures, liver tissue specimens were examined under a light microscope. The levels of ALT, AST, total bilirubin, SOD, GSH-Px and MDA were significantly increased in rats exposed to cigarette smoke compared with those of the controls. Light microscopic examination of liver specimens from rats exposed to cigarette smoke revealed mononuclear cell infiltration and that some of the hepatocytes had a hyperchromatic nucleus and enlarged sinusoids. The rats which were treated with CAPE along with cigarettes had partially attenuated histological changes associated with cigarette exposure. In conclusion, the damage inflicted by cigarette in the rat liver can be partially prevented by CAPE administration.