COMPARATIVE EFFECTS OF CHRONIC ADMINISTRATION OF SOME PSYCHOTROPIC-DRUGS ON RAT-BRAIN CORTEX ACETYLCHOLINESTERASE ACTIVITY

1. The response of central cholinergic neurotransmission to the chronic administration of some psychotropic drugs to rats was investigated using brain acetylcholinesterase activity as a neurochemical marker for cholinergic neurons

ALTERATIONS IN SOME LIPID COMPONENTS AND CA-2+ ATPASE ACTIVITY IN BRAIN OF RATS FED AN ATHEROGENIC DIET

Male Wistar rats were fed an atherogenic diet for four months to investigate possible diet-induced lipid alterations and brain Ca2+ ATPase activity. Total cholesterol and triglyceride levels were found to be increased significantly in both serum and brain while the phospholipid level was decreased in both. The distribution of serum cholesterol between high-density and low-density lipoproteins was altered when compared to control rats with a decrement in HDL-cholesterol and a pronounced increment in LDL-cholesterol. The atherogenic diet resulted in about 50% depression in brain Ca2+ ATPase activity. It is concluded that alterations in ion transport and neurotransmitter release may be expected due to pronounced inhibition of brain Ca2+ ATPase activity in rats fed an atherogenic diet

Nitric oxide-mediated regulation of gastric H+, K+-ATPase and alcohol dehydrogenase following ethanol-induced injury in rats

The mucosal protective effect of nitric oxide (NO) was examined by using NG-nitro-L-arginine methyl ester (L-NAME) as nitric oxide synthase (NOS) inhibitor and nitroprusside (NP) as NO donating agent, in ethanol-induced rat gastric lesion model. The results are summarized as follows: (1) As gastric tissue samples were examined by light microscopy, intragastric exposure of ethanol was demonstrated to induce gastric injury; which was more prominent in female rats. The depletion of NO by L-NAME treatment exacerbated the ethanol-induced gastric lesion but NP together with ethanol promoted repair of the mucosal injury, especially in female rats. (2) Gastric H+, K+-ATPase enzyme activity, which was responsible for acid secretion, seemed not to be effected by ethanol treatment. Together with ethanol, L-NAME treatment activated, whereas NP treatment inhibited, the enzyme activity in female rats. (3) Ethanol treatment inhibited gastric alcohol dehydrogenase (ADH) activity, which was responsible for the first-pass metabolism of ethanol. Together with ethanol, L-NAME did not effect the enzyme activity whereas NP treatment disappeared the inhibitory effect of ethanol in both gender. Hydroxyl radical (OH .) scavenger activity was found to increase in ethanol and ethanol + NP groups in both sexes, but superoxide radical (O-2(-.)) scavenger activity did not change. The results indicate that NO may ameliorate the damaging effect of ethanol possibly by regulating acid secretion, ethanol metabolism, and antioxidant content in rat gastric mucosa

RELATIONSHIP OF SOME ENDOGENOUS SEX STEROID-HORMONES TO LEUKOCYTE ARYLSULFATASE-A ACTIVITIES IN PREMENOPAUSAL AND POSTMENOPAUSAL HEALTHY WOMEN

This study was planned to investigate whether the physiological variations in endogenous gonadal steroid hormones during fertile period to menopause might affect the Arylsulphatase A (ARS-A) activities in leukocytes in healthy women. In premenopausal women, means of the leukocyte ARS-A activity were significantly highest at ovulatory phase, and lowest at early follicular phase. In contrast, the mean leukocyte ARS-A activity in postmenopausal women was approximately equivalent to the mean leukocyte enzyme in cycling women at early follicular phase in whom the lowest enzymatic activity was observed. The results of our study, therefore, concluded that gonadal steroid released physiologically into the bloodstream might be expected to stimulate the lysosomal system thereby leading to an enhancement in leukocyte ARS-A activity

Ebselen as protection against ethanol-induced toxicity in rat stomach

The mucosal protective effect of ebselen was examined in an ethanol-induced rat gastric lesion model. Examination of gastric tissue samples by light microscopy showed that i.g, exposure to 50% ethanol induced gastric injury, which was mon prominent in female rats. Ethanol did not effect the gastric acid secretion examined by means of H+-K(+)ATPase. the increment of which might be harmful in the stomach, But ebselen with or without ethanol kept H+-K(+)ATPase below control levels. Gastric alcohol dehydrogenase (ADH) was mainly responsible for oxidation of ethanol in the stomach before it enters the bloodstream I.g. ethanol exposure inhibited the ADH activity but ebselen eliminated the ethanol-induced inhibition of this enzyme. Therefore, ebselen exhibited a beneficial effect by increasing the gastric ethanol metabolism and by ameliorating the possible tissue toxicity of ethanol. Consistently, we also found that ebselen diminished the blood ethanol level. A gender difference in the blood ethanol levels existed following the same dose of ethanol but then was no difference in ADH activity. Histologically, mucosal injury following ebselen exposure together with ethanol was less severe compared with ethanol treatment alone. We concluded that the decrease in ethanol-induced mucosal injury following ebselen may have contributed to the inhibition of H+-K(+)ATPase and the activation of ADH by ebselen

Prolidase I activity in liver tissue: Effects of ethanol and selenium

Selenium is an important factor as a component of glutathione peroxidase. In circumstances like chronic alcoholism, involving increased activity of free radicals, selenium deficiency can augment tissue degeneration by enhancing lipid peroxidation. In the present study, selenium was given to rats fed an alcohol-rich diet and the extent of liver injury was assessed by measuring prolidase I activity as well as hydroxyproline and free proline levels in the liver tissue after five months of ethanol ingestion. These findings were compared with the levels in controls and in the rats receiving sodium selenite in addition to ethanol. Hepatic prolidase activity increased in both groups receiving alcohol. There was no change in tissue hydroxyproline levels. We conclude that tissue (or serum) prolidase I activity may be useful for the early detection of alcoholic liver injury or other forms of oxidant-induced liver damage

The changes in serum nitric oxide levels in rats undergoing laparoscopic versus open bilateral truncal vagotomy

Laparoscopic surgery necessitates the description and definition of the various biochemical and physiological effects of pneumoperitoneum in the body. We report the preliminary results of an experimental study investigating the changes in serum nitric oxide levels in rats undergoing laparoscopic (LBTV) versus open (OBTV) bilateral truncal vagotomy. Thirty-six Wistar-albino rats were divided into 3 groups including the control (n:6), laparoscopy (n:15) and open (n:15) group. Controls underwent laparotomy with a 5 cm midline incision and were sacrificed after blood was drawn from inferior vena cava for baseline values. LBTV was effected with 3 mini-trocars. Pneumoperitoneum was maintained at 6-7 mm Hg. OBTV was performed with a 5 cm midline incision. Both of the procedures lasted 30-35 minutes. In each group, laparotomy was performed either 6 hours (n:5), 12 hours (n:5), or 24 hours (n:5) after the first operation and blood for analysis was obtained by puncturing inferior vena cava. Serum NO2-/NO3- (stabile end-products of NO) levels were determined spectrophotometrically by the Griess reaction, As a results, serum nitrate and nitrite levels were found to be depressed on both the LBTV and OBTV groups at 12 hours compared to controls, however, this difference was statistically significant only in the OBTV group (6.79 +/- 0.81 mu M versus 16.46 +/- 7.43 mu M, respectively: p 0.05, Mann-Whitney U). These preliminary results suggest that bilateral truncal vagotomy performed by the open technique inhibits NO synthetase in contrast to laparoscopic bilateral truncal vagotomy. This effect may be attributable to inhibitory mediatory released from the larger trauma in the open procedure