Effect of cigarette smoke and alpha-tocopherol (vitamin E) on fertilization, cleavage, and embryo development rates in mice: an experimental in vitro fertilization mice model study.

OBJECTIVE: The objective was to elucidate the effects of cigarette smoke per se or vitamin E on mice exposed to cigarette smoke, with regard to fertility and cleavage rates, and embryo development in an experimental in vitro fertilization (IVF) mice model. STUDY DESIGN: Female and male mice, weighing 18-25 g and aged 14-16 weeks, were separated and divided into cigarette smoke-exposed (SE) and non-smoke-exposed (NSE) groups. A specially designed cage with a cigarette smoking machine was constructed. The SE (20 cigarettes/day) group was put in the cage for 10 weeks. SE and NSE female and male mice were given 50mg/kg of vitamin E intraperitoneally for 10 weeks and were cross-mated thereafter so as to produce seven different subgroups of mice population as follows: group I-NSE male and female mice (control); group II-SE female mice and NSE male mice; group III-NSE female with SE male mice; group IV-SE male and SE female mice; group V-SE female mice treated with vitamin E and SE only male mice; group VI-SE only female and male mice treated with vitamin E; and finally group VII-vitamin E-treated SE male and female mice. Following superovulation with FSH, follicles of female mice were obtained via laparotomy under high-dose ether. Male mice testicles were retrieved via the same surgical procedure. Both gametes were obtained and used for IVF. Fertilization, cleavage rates, and day 3 embryo grading were assessed in four groups. RESULTS: With regard to fertilization rate, group II (36%) significantly differed from group I (85%, p=0.002), group III (68.7%, p=0.04), but not from group IV (20.6%, p=0.34). Taking embryo development rate into consideration, group II (32%) had a lower percentage of embryo development compared with group I (75%, p<0.01) and group III (62.5%, p<0.001), but not group IV (17.2%, p=0.42). Percentages of embryo cleavage, embryo development, and day 3 grade I embryos did differ among four of the groups (p>0.05). CONCLUSIONS: Fertilization and cleavage rates were mainly affected in the SE female mice population. The impact of vitamin E on fertilization, cleavage, and embryo development rates was not relevant among SE male and SE female mice.

Effect of nitric oxide inhibition on rat liver ischemia reperfusion injury.

Objective: to determine the role of nitric oxide (NO) in rat liver ischemia reperfusion we examined the effects of competitive NO synthesis inhibitor L-nitro-arginine-methyl-ester (L-NAME) and NO precursor L-arginin. Methods: 46 Sprague-Dawley rats were divided into five groups. Group 1, sham operated; group 2, 30-min ischemia administered; group 3, 60-min reperfusion administered after ischemia; group 4, 50 mg/kg L-NAME was given i.v. immediately before reperfusion; group 5, 50 mg/kg L-NAME+250 mg/kg L-arginin was given i.v. immediately before reperfusion. At the end of the experiment, liver was removed and superoxide dismutase (SOD), catalase, and malondialdehyde (MDA) were measured, transaminases SGOT and SGPT were measured in sera. Liver was also evaluated histopathologically. Results: transaminase levels were the highest in ischemia reperfusion group. Transaminases in this group were high compared with sham, ischemia, L-NAME and L-arginin groups (***P<0.001, ***P<0.001, *P<0.05, *P<0.05, respectively). SOD activity was 29.8+4 U/mg protein in L-arginin group. This level was the lowest level in all groups. SOD activity in L-arginin group was lower than that of sham and ischemia reperfusion groups (**P<0.01, *P<0.05, respectively). There were no significant differences in catalase activity and MDA levels among groups. Tissue damage was significant in ischemia and ischemia reperfusion groups. Tissue damages in these groups were greater than that of sham group (***P<0.001). In L-NAME treated group, tissue damage was similar to sham group, and significantly less than ischemia reperfusion group and L-arginin group (**P<0.01). Conclusion: even though there was significant tissue damage, we have not observed oxidative stress in the length of ischemia reperfusion period that we have performed. Mechanism of this damage seems to be independent from lipid peroxidation. NO supplementation decreased SOD, but did not cause further tissue damage. NO may dispose O(2)(-) by formation of peroxynitrite. L-NAME did not change lipid peroxidation, but clearly reduced reperfusion injury.

Ovarian, uterine and brain mast cells in female rats: cyclic changes and contribution to tissue histamine.

Using histochemical techniques, we determined mast cell content in ovarian, uterine and brain tissues throughout the estrus cycle of the rat. In one series of experiments, 26 cycling female rats were used for the measurement of follicle stimulating hormone (FSH) in plasma and evaluation of mast cells in the tissues. In a second series, cycling female rats were used for the determination of tissue histamine. The number, degranulation pattern and staining characteristics of mast cells changed synchronously in rat ovarian, uterine and brain tissues during the estrus cycle. A great majority of mast cells in tissues were stained by Alcian blue at proestrus and metestrus. Safranin-stained mast cells were abundant in all tissues during estrus and diestrus. Alcian blue-stained mast cells contribute to the change of tissues histamine level. In ovarian tissue, histamine level increased significantly at proestrus and metestrus. The lowest ovarian histamine level was determined at estrus, in which virtually all mast cells were stained by safranin only. Mast cells in ovarian, uterine and brain tissues seem to change their histamine content throughout the estrus cycle. Mast cells are absent from the thalamus during proestrus and are present in the hypothalamus only during the estrus phase. Plasma FSH concentrations (mlU ml-1) did not significantly change throughout the estrus cycle (proestrus: 0.81 +/- 0.11, estrus: 0.69 +/- 0.07, metestrus: 0.82 +/- 0.13, diestrus: 0.67 +/- 0.19).

The effect of vasoactive intestinal peptide (VIP) on mast cell invasion/degranulation in testicular interstitium of immobilized + cold stressed and beta-endorphin-treated rats.

The effect of VIP on mast cell invasion/degranulation in testicular interstitium of stressed (immobilization and cold) and beta-endorphin-treated rats were investigated. Fifty-three Wistar male rats were used in four series of experiments. Initially, the effect of immobilization and cold stress on mast cell invasion and degranulation in testicular interstitium was examined in three age group of rats: 15 (n = 6), 30 (n = 6), and 45 (n = 7) days of age. Five animals per age group were used as controls. Because the most obvious effect of the stress on mast cell invasion/degranulation in testicular interstitium was observed in 45-day-old rats, the action of VIP in stressed and beta-endorphin-treated rats was only investigated at this age group. Mast cells and Leydig cells were evaluated by using histochemical and light microscopic protocols. Stress caused mast cell accumulation and degranulation in the testicular interstitium. Stress decreased heparin synthesis and possibly increased histamine content of mast cells. The effect of beta-endorphin was not as high as seen with stress. In some areas of testicular interstitium of stressed rats, there were aplasic and/or inactive Leydig cells. VIP inhibited proliferation and degranulation of mast cells, increased heparin content of the cells, and protected Leydig cells. By way of mast cell accumulation and degranulation in the testicular interstitium, exposure to stress may lead to Leydig cell damage and infertility. VIP may be involved in the protection of normal testicular function under stress conditions.

The effect of vasoactive intestinal peptide (VIP) on superoxide dismutase and catalase activities in renal tissues of rats exposed to hemorrhagic ischemia-reperfusion.

The effect of vasoactive intestinal peptide (VIP) on the activities of superoxide dismutase and catalase was investigated in renal tissues of rats exposed to 30% hemorrhage followed by reperfusion. In addition to enzyme activities, renal tissues were also histologically evaluated. Thirty percent hemorrhage had no significant effect on the activity of either enzyme. Reperfusion altered the activity of renal catalase but not of superoxide dismutase. On the other hand, administration of VIP (25 ng.kg-1) together with shed blood retransfusion protected the renal tissue from hemorrhagic ischemia-reperfusion injury without increasing superoxide dismutase and catalase activity. These results seem to be related either to the inhibitory effect of VIP on production or quenching activity of some reactive oxygen species. In conclusion, VIP may be a novel promising therapeutic approach toward defenses against hemorrhagic ischemia-reperfusion injury as an antioxidant.

Calcitonin inhibits heterotopic bone formation in rats.

The effect of salmon calcitonin on heterotopic bone formation in rats was analysed. Thirty days after implantation of demineralized bone matrix, the weights of implants from animals receiving calcitonin were reduced, in contrast to the increase shown in the untreated control group. In the control group, the implants were visible on roentgenograms at the 20th day and histologic examination revealed new bone formation, whereas in the calcitonin-treated group the implants were never visible on roentgenograms throughout the study and only remnants of implants could be detected histologically. This study suggests that calcitonin inhibits heterotopic bone formation in rats.

Effect of vasoactive intestinal peptide and naloxone combination on urinary N-acetyl-beta-D-glucosaminidase level and kidney histology of rats exposed to severe hemorrhage.

Renal hypoperfusion which occurs in hemorrhagic shock creates an environment in which cellular injury and organ dysfunction can occur during the episode of shock as well as reoxygenation and reperfusion. At the same time, mast cell degranulation which is observed during hemorrhage may have an additional deleterious effect on the kidney. Twenty-two (Mus norvegicus albinos) rats (200-250 g) of either sex were used. The animals were divided into three groups. Group 1, the control group, was exposed to a 40% hemorrhage. Group 2 was exposed to 40% hemorrhage and then shed blood reperfused. Group 3 was exposed to 40% hemorrhage, and in addition to shed blood reperfusion 25 ng kg-1 vasoactive intestinal peptide (VIP) + 5 mg kg-1 naloxone (NLX) were given. At the end of the experiment the kidneys were evaluated either histologically or by measurement of the urinary N-acetyl-beta-D-glucosaminidase (NAG) activity. Shed blood reperfusion caused continuation of ischemic tissue damage and elevation of urinary NAG activity. Addition of VIP and NLX to the blood reperfusion caused a decrease in urinary NAG excretion, and the histology of renal tissue was almost normal.

The effect of vasoactive intestinal peptide (VIP) and naloxone combination on survival rates in rats exposed to severe hemorrhage.

In this experiment, the effects of different doses of vasoactive intestinal peptide (VIP) and naloxone (NLX) combinations on survival rates were investigated in rats exposed to 40% hemorrhage. A combination of 25 ng.kg-1 VIP+5 mg.kg-1 NLX showed the best results on survival. The important prospect of this combination is to have the most potent inhibitory effect on mast cell degranulation. When this combination was given together with shed blood reperfusion and 7.5% NaCl, survival rate increased relative to the administration of shed blood alone and of 7.5% NaCl. These findings suggest that inhibition of mast cell degranulation has a beneficial effect on severe hemorrhage.

[The effects of ciprofloxacin and ofloxacin on the cellular and humoral immune response in mice]. / Siprofloksasin ve ofloksasinin farelerde hücresel ve hümoral immün cevap üzerine etkileri.

The effects of a 7 days chemotherapy with ciprofloxacin or ofloxacin on the cellular and humoral immune responses in albino mice were studied. The non-toxic doses of the drugs (10 or 30 mg/kg/day) were used. The delayed-type hypersensitivity reaction to sheep blood cells and skin biopsy were evaluated for cellular immune response. The complement fixation method was applied for the determination of the humoral immune response. Both drugs increased the cellular and humoral immune responses.

[The effects of ciprofloxacin on intestinal flora and Paneth cells]. / Siprofloksasinin barsak florasi ve paneth hücrelerine etkileri.

The effects of ciprofloxacin were investigated on colonic microbial flora and Paneth cells in eight healthy albino rabbits following a 10 mg intravenous dose. Two rabbits were used as control group. Aerobic fecal cultures were negative on rabbits of experiment. Vacuolisation and reduction of eosinophilic fields were seen in Paneth cells by light microscopic examination.

Mast cell degranulation in hemorrhagic shock in rats and the effects of vasoactive intestinal peptide, aprotinin and H1 and H2-receptor blockers on degranulation.

Various stressful stimuli cause mast cell degranulation. Hemorrhagic shock is one such stressful stimulus which may cause mast cell degranulation and histamine release. Histamine may be involved in the pathophysiology of hemorrhage. It was reported that there are large amounts of histamine in the anterior and posterior lobes of the pituitary and the adjacent median eminence of the hypothalamus. Most of the histamine in the posterior pituitary is in mast cells. In addition, both vasoactive intestinal peptide (VIP) and histamine-containing neurons are available in the hypothalamus. It therefore seems reasonable to suppose that these three systems (i.e., mast cells, VIP-containing neurons, and histamine-containing neurons) may play an important role in the progression of hemorrhagic shock. 66 albino rats (200-250 g) of either sex were used. The presence of mast cells was examined by light microscopy. Hemorrhage caused mast cell degranulation in a correlation with the amount of blood loss. In all cases, the most intense degranulation was observed in the hypothalamus, especially the nucleus arcuatus, and in the subcutaneous tissue. The intensity of degranulation gradually decreased in the peripheral blood vessel, peritoneum and omentum, in this order. VIP prevented degranulation, but aprotinin and H1 and H2 receptor blockers did not.

Effects of various acidic and alkaline solutions used to dissolve urinary calculi on the rabbit urothelium.

It is well known that infection-induced stones (apatite, struvite), uric acid and cystine calculi in the urinary tract can be managed by the use of certain chemical solutions. We investigated the effects of various acidic and alkaline solutions on the rabbit urothelium. Acidic solutions (pH: 4.2) caused more urothelial injury as compared to alkaline solutions (pH: 7.6). Ureteral injury was more severe than the bladder injury. Magnesium-containing solutions caused less injury to the urothelium.