46 research outputs found
Učinak trotjednog davanja suplemenata cinka i melatonina na oksidacijski-antioksidacijski sustav u eksperimentalnoj bubrežnoj ishemiji-reperfuziji kod štakora
Renal ischemia-reperfusion directly affects glomerular and tubular epithelium. Oxygen free radicals have a significant part in the pathophysiology of renal ischemia-reperfusion injury. The present study aimed to identify the effects of 3-week zinc, melatonin, and zinc + melatonin supplementation on malondialdehyde (MDA) levels in tissue and plasma and glutathione levels (GSH) in erythrocytes and tissue of rats with experimentally induced renal ischemia-reperfusion injury. The study included Wistar albino rats with a mean weight of 250 g. Study groups were formed as follows: control, sham-control, ischemia + reperfusion, zinc + ischemia-reperfusion, melatonin + ischemia-reperfusion, and zinc + melatonin + ischemia-reperfusion. Animals were supplemented with zinc and melatonin 3 mg/kg/day i.p. for 3 weeks before the induction of ischemia-reperfusion. Renal ischemia-reperfusion was induced in the left kidney under general anesthesia and consisted of ischemia for 45 minutes and reperfusion for 1 hour. After the procedure, animals were sacrificed and blood and kidney samples were collected to analyze MDA and GSH levels. GSH values in kidney tissues and erythrocytes were found to be elevated in the groups supplemented with zinc and melatonin (p<0.005). When MDA values in renal tissue and plasma were examined, it was seen that ischemia significantly elevated this parameter, while zinc and melatonin supplementation significantly inhibited MDA values (p<0.002). The results of the study indicated that oxidative injury of the blood and renal tissues of rats increased in association with ischemia-reperfusion, but zinc and melatonin supplementation before ischemia-reperfusion markedly reduced this oxidative damage.Bubrežna ishemija-reperfuzija izravno djeluje na glomerularni i tubularni epitel. Slobodni radikali kisika imaju značajnu ulogu u patofiziologiji bubrežne ishemijsko-reperfuzijske ozljede. Cilj ovoga ispitivanja bio je utvrditi učinke trotjednog davanja suplemenata cinka, melatonina i cinka + melatonina na tkivne i plazmatske razine malondialdehida (MDA) te na razine razine glutationa (GSH) u eritrocitima i tkivu štakora s eksperimentalno izazvanom bubrežnom ishemijsko-reperfuzijskom ozljedom. Ispitivanje je provedeno na Wistar albino štakorima srednje težine 250 g podijeljenim u sljedeće
skupine: kontrolna, lažno kontrolna, ishemija + reperfuzija, cink + ishemija-reperfuzija, melatonin + ishemija-reperfuzija i cink + melatonin + ishemija-reperfuzija. Životinje su dobivale suplemente cinka i melatonina, 3 mg/kg/dan i.p. kroz 3 tjedna prije negoli je izazvana ishemija-reperfuzija. Bubrežna ishemija-reperfuzija izazvana je u lijevom bubregu u općoj anesteziji, a sastojala se od ishemije u trajanju od 45 minuta i reperfuzije u trajanju od 1 sata. Nakon zahvata životinje su žrtvovane, a uzorci krvi i bubrega uzeti su za analizu razina MDA i GSH. Vrijednosti GSH u bubrežnom tkivu i eritrocitima bile su povišene u skupinama koje su dobivale suplemente cinka i melatonina (p<0,005). Ispitivanje vrijednosti MDA
u bubrežnom tkivu i plazmi pokazalo je da je ishemija značajno povisila ovaj parametar, dok je davanje suplemenata cinka i melatonina značajno inhibiralo vrijednosti MDA (p<0,002). Rezultati ove studije pokazali su da se oksidativno oštećenje u krvi i bubrežnom tkivu štakora povećalo uz ishemiju-reperfuziju, ali je davanje suplemenata cinka i melatonina prije ishemije-reperfuzije znatno smanjilo oksidativno oštećenje
Effect of testosterone supplementation on leptin release in rats after castration and/or unilateral surrenalectomy
Wstęp: Celem badania była ocena wpływu suplementacji testosteronu na uwalnianie leptyny u szczurów poddanych kastracji i jednostronnej
adrenalektomii.
Materiał i metody: Badanie przeprowadzono na 80 dorosłych samcach szczurów Wistar Albino. Zwierzęta podzielono na 8 grup, po 10
w każdej grupie, w następujący sposób: grupa 1. — grupa kontrolna, grupa 2. — suplementacja testosteronu, grupa 3. — kastracja, grupa
4. — adrenalektomia, grupa 5. — kastracja i adrenalektomia, grupa 6. — kastracja i suplementacja testosteronu, grupa 7. adrenalektomia
i suplementacja testosteronu, grupa 8. — kastracja, adrenalektomia i suplementacja testosteronu. Zwierzętom z grup 2., 6., 7. i 8. podawano
domięśniowo 5 mg/kg mc./d. propionianu testosteronu przez 4 tygodnie. Pobrano próbki krwi na oznaczenie stężeń leptyny, LH, FSH
i wolnego oraz całkowitego testosteronu w osoczu.
Wyniki: U zwierząt z grup 3. i 5. stężenia leptyny i LH były wyższe niż w pozostałych grupach (p < 0,01). Stężenia leptyny i LH w grupach
1. i 4. były wyższe niż w grupach 2., 6., 7. i 8. (p < 0,01). Porównanie badanych grup pod względem stężeń FSH w osoczu wykazało, że
parametr ten przyjmował istotnie większe wartości w grupach 3. i 5. niż w pozostałych grupach (p < 0,01). Stężenia FSH w grupach 1.
i 4. były niższe niż w pozostałych (p < 0,01). Najwyższe stężenia testosteronu zaobserwowano w grupach 2., 6., 7. i 8. (p < 0,01). Stężenia
testosteronu w grupach 1. i 4. były wyższe niż w grupach 3. i 5. (p < 0,01).
Wnioski: Wyniki badania wskazują, że jednostronna adrenalektomia u szczurów nie wpływa istotnie na wydzielanie leptyny. Sugerują
również, że stężenie LH w osoczu silniej oddziałuje na osoczowe stężenie leptyny niż stężenie testosteronu. (Endokrynol Pol 2012; 63 (2): 119–124)Introduction: The objective of this study was to examine the effect of testosterone supplementation on leptin release in rats which underwent
castration and unilateral surrenalectomy.
Material and methods: The study was conducted on 80 adult male Wistar albino rats. Animals were divided into eight groups, with
ten animals in each group. Group 1 was the Control group, Group 2 the Testosterone group, Group 3 the Castration group, Group 4 the
Surrenalectomy group, Group 5 the Castration and Surrenalectomy group, Group 6 the Castration and Testosterone group, Group 7 the
Surrenalectomy and Testosterone group, and Group 8 the Castration, Surrenalectomy and Testosterone group. The animals in Groups 2, 6,
7 and 8 were administered 5 mg/kg/day intramuscular testosterone propionate for four weeks. Blood samples were collected for analyses
of leptin, LH, FSH and free and total testosterone levels in plasma.
Results: Groups 3 and 5 had the highest leptin and LH levels of all the groups (p < 0.01). Leptin and LH levels in Groups 1 and 4 were
higher than those in Groups 2, 6, 7 and 8 (p < 0.01). A comparison of groups with regard to plasma FSH levels showed that the concerned
parameter was significantly higher in Groups 3 and 5 than in the other groups (p < 0.01). FSH levels in Groups 1 and 4 were lower than
those in all other groups (p < 0.01). The highest testosterone levels were obtained in Groups 2, 6, 7 and 8 (p < 0.01). Testosterone levels in
Groups 1 and 4 were higher than those in Groups 3 and 5 (p < 0.01).
Conclusions: This study demonstrates that unilateral surrenalectomy in rats does not have a significant effect on leptin release, while
plasma LH levels, rather than testosterone, may be more effective on plasma leptin. (Pol J Endocrinol 2012; 63 (2): 119–124
Pre- and post-estrogen administration in global cerebral ischemia reduces blood-brain barrier breakdown in ovariectomized rats
The aim of present study was to determine the effect of estrogen treatment on blood-brain barrier permeability in rats with induced global cerebral ischemia. The study included six-month-old female Sprague-Dawley rats which were divided into the following groups: Control-Ischemia-Reperfusion (C + I-R); Ovariectomy-Ischemia-Reperfusion (Ovx + I-R); Ovariectomy + Estrogen + Ischemia-Reperfusion (Ovx + E + I-R); Ovariectomy + Ischemia-Reperfusion + Estrogen (Ovx + I-R + E). Ischemia-reperfusion was induced by clamping two carotid arteries, then opening the clamp. Blood-brain barrier permeability was visualized by Evans Blue extravasation and quantified by spectrophotometry. Our results indicate that following ischemia-reperfusion the BBB permeability is increased in ovariectomized rats (Evans Blue extravasation) compared to the control group in the cortex, thalamus, hippocampus, cerebellum and brain stem, while in the midbrain no significant increase was detected. In contrast, BBB permeability in the groups treated with estrogen, administered either before or after ischemia-reperfusion, was significantly lower than in ovariectomized animals. In conclusion, the increase in BBB permeability resulting from experimentally induced cerebral ischemia was prevented by exogenous estrogen treatment. The study results indicate that estrogen may be used for therapeutic purposes in ischemia-reperfusion
Interactive effects of melatonin, exercise and diabetes on liver glycogen levels
Background: This study aimed to examine the effects of melatonin supplementation on liver glycogen levels in rats with streptozotocin-
induced diabetes and subjected to acute swimming exercise.
Material and methods: Eighty Sprague-Dawley type adult male rats were divided into eight groups: Group 1, general control; Group 2,
melatonin-supplemented control; Group 3, melatonin-supplemented diabetes; Group 4, swimming control; Group 5, melatonin-supplemented
swimming; Group 6, melatonin-supplemented diabetic swimming; Group 7, diabetic swimming; Group 8, diabetic control.
Melatonin was supplemented at a dose of 3 mg/kg/day intraperitoneally for four weeks. Liver tissue samples were collected and evaluated
using a Nikon Eclipse E400 light microscope. All images obtained from the light microscope were transferred to PC medium and evaluated
using Clemex PE 3.5 image analysis software.
Results: The lowest liver glycogen levels in the study were found in group 4. Liver glycogen levels in groups 3, 6, 7 and 8 (the diabetic
groups) were higher than group 4, but lower than those in groups 1 and 2. The lowest liver glycogen levels were obtained in groups 1 and 2.
Conclusions: The study indicates that melatonin supplementation maintains the liver glycogen levels that decrease in acute swimming
exercise, while induced diabetes prevents this maintenance effect in rats. (Pol J Endocrinol 2011; 62 (3): 252–255)Background: This study aimed to examine the effects of melatonin supplementation on liver glycogen levels in rats with streptozotocin-
induced diabetes and subjected to acute swimming exercise.
Material and methods: Eighty Sprague-Dawley type adult male rats were divided into eight groups: Group 1, general control; Group 2,
melatonin-supplemented control; Group 3, melatonin-supplemented diabetes; Group 4, swimming control; Group 5, melatonin-supplemented
swimming; Group 6, melatonin-supplemented diabetic swimming; Group 7, diabetic swimming; Group 8, diabetic control.
Melatonin was supplemented at a dose of 3 mg/kg/day intraperitoneally for four weeks. Liver tissue samples were collected and evaluated
using a Nikon Eclipse E400 light microscope. All images obtained from the light microscope were transferred to PC medium and evaluated
using Clemex PE 3.5 image analysis software.
Results: The lowest liver glycogen levels in the study were found in group 4. Liver glycogen levels in groups 3, 6, 7 and 8 (the diabetic
groups) were higher than group 4, but lower than those in groups 1 and 2. The lowest liver glycogen levels were obtained in groups 1 and 2.
Conclusions: The study indicates that melatonin supplementation maintains the liver glycogen levels that decrease in acute swimming
exercise, while induced diabetes prevents this maintenance effect in rats. (Pol J Endocrinol 2011; 62 (3): 252–255
Leptin and zinc relation : In regulation of food intake and immunity
Leptin is synthesized and released by the adipose tissue. Leptin, which carries the information about energy reserves of the body to the brain, controls food intake by acting on neuropeptide Y (NPY), which exercises a food-intake-increasing effect through relevant receptors in the hypothalamus. Zinc deficiency is claimed to result in anorexia, weight loss, poor food efficiency, and growth impairment. The fact that obese individuals have low zinc and high leptin levels suggests that there is a relation between zinc and nutrition, and consequently also between zinc and leptin. Leptin deficiency increases the predisposition to infections and this increase is associated with the impairments in the production of cytokines. Zinc has a key role in the sustenance of immune resistance against infections. Dietary zinc deficiency negatively affects CD +4 cells, Th functions, and consequently, cell-mediated immunity by causing a decrease in the production of IL-2, IF-γ, and TNF-α, which are Th1 products. The relation between zinc and the concerned cytokines in particular, and the fact that leptin has a part in the immune responses mediated by these cytokines demonstrate that an interaction among cellular immunity, leptin and zinc is inevitable. An overall evaluation of the information presented above suggests that there are complex relations among food intake, leptin and zinc on one hand and among cellular immunity, leptin and zinc on the other. The aim of the present review was to draw attention to the possible relation between zinc and leptin in dietary regulation and cellular immunity