Biomedical subjects

Akcahan Gepdiremen

Publications and source records attributed to Akcahan Gepdiremen.

5 recordsLinked to original sources

PubMed2006

The effect of L-carnitine in the prevention of ionizing radiation-induced cataracts: a rat model.

BACKGROUND: The objective was to determine the antioxidant role of L-carnitine (LC) against ionizing radiation-induced cataracts in lens after total cranium irradiation of rats with a single dose of 5 Gy. METHODS: Sprague-Dawley rats were used in this experiment and were divided into three groups. Group 1 did not receive LC or irradiation (control group). Group 2 received a 5 Gy gamma irradiation as a single dose to the total cranium (RT group). Group 3 received total cranium irradiation plus 100 mg/kg body weight/day LC (RT+LC group). The rats were irradiated using a cobalt-60 teletherapy unit. At the end of the 10th day, the rats were sacrificed and their eyes were enucleated. The lenticular activity of the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured. Furthermore, the lenticular content of an indicator of lipid peroxidation, malondialdehyde (MDA), was measured. RESULTS: Irradiation significantly increased the MDA level as an end product of lipid peroxidation. Irradiation also significantly decreased SOD activity and increased GSH-Px activity, indicating the generation of oxidative stress and an early protective response to oxidative damage. Irradiation with 5 Gy to the total cranium as a single fraction formed cataracts in the rat lenses. Cataract development was detectable in 9 rats in the RT group, and in only 4 rats in the RT+LC group 10 days after irradiation. LC administration plus irradiation significantly decreased the MDA level and increased the activity of SOD and GSH-Px enzymes, which might indicate the protection of the lenses from gamma radiation-induced cataracts. CONCLUSIONS: L-carnitine may protect against the damage produced by gamma radiation by increasing the activity of the SOD enzyme and by scavenging free radicals generated by ionizing radiation. As a result of this process, MDA as an indicator of lipid peroxidation may decrease.

Animals↗

PubMed2006

Protective effect of L-carnitine against bilirubin-induced neuronal cell death.

There is growing evidence that glutamate receptor-mediated injury plays a crucial role in bilirubin neurotoxicity. L-carnitine (LC) has been shown to prevent glutamate-induced toxicity in neuronal cell culture. The purpose of this study is to assess whether LC is able to prevent bilirubin neurotoxicity. Unconjugated bilirubin at different concentrations was administered to cerebellar granular cell cultures prepared from 1-day-old Sprague-Dawley rats. The neuroprotective effect of LC was examined. LC at doses of 10(-6), 10(-5), 10(-4) and 10(-3) M was applied to culture flasks. LC at a dose of 10(-4) M significantly blocked bilirubin neurotoxicity. On the other hand, LC significantly increased bilirubin toxicity at a higher dose (10(-3) M). LC at the doses of 10(-5) and 10(-6) M was found to be ineffective. 10(-4) M LC decreased bilirubin-induced neuronal cell death from 47.72+/-3.68 to 27.23+/-5.14%, (P=0.003). The present study demonstrates, for the first time, that LC protects against bilirubin neurotoxicity in a dose-dependent manner in cerebellar granular cell culture of rats. Further research is needed to confirm our findings and to clarify the mechanisms responsible for the protective effect of LC.

Animals↗

PubMed2005

L-carnitine protects against glutamate- and kainic acid-induced neurotoxicity in cerebellar granular cell culture of rats.

Glutamate mediated intracellular calcium accumulation and free radical generation are thought to be major mechanisms that contribute to cell death in hypoxic-ischemic brain injury. For this reason, various glutamate receptor antagonists and antioxidants have been investigated for their therapeutic potential. To assess whether L-carnitine, a possible antioxidant, is able to prevent glutamate- and kainic acid (KA)-induced neurotoxicity. Glutamate (10(-7) M) and one of its receptor agonists, KA (10(-4) M) were administered to cerebellar granular cell cultures that were prepared from 1-day-old Sprague-Dawley rats. The neuroprotective effect of L-carnitine was examined. L-carnitine at doses of 10(-6), 10(-5), 10(-4), 10(-3) M was applied to culture flasks. L-carnitine at doses of 10(-4) and 10(-3) M significantly blocked glutamate-induced neurotoxicity. 10(-4) M dose of L-carnitine proved to be more effective than 10(-3)M. L-carnitine also blocked KA-induced neurotoxicity only at the dose of 10(-4) M. 10(-4) M L-carnitine, the most effective dose in both glutamate- and KA-induced neurotoxicity, decreased glutamate-induced neuronal cell death from 36.14+/-2.95% to 17.59+/-2.25%; (P<0.001) and KA-induced neuronal cell death from 21.4+/-0.41 to 13.4+/-1.38%; (P<0.001). The present study demonstrates that L-carnitine protects against glutamate- and KA-induced neurotoxicity. Protective effect of L-carnitine may result from its antioxidant activity because free radical generation is a common result in either glutamate- or KA-induced neurotoxicity. L-carnitine merits further investigation as a therapeutic option in hypoxic-ischemic brain injury of newborn.

Animals↗

PubMedDate not supplied

Apolipoprotein E polymorphism and stroke in a population from eastern Turkey.

Human apolipoprotein E (apo E) alleles are polymorphic with significantly different frequencies among different ethnic groups and have been associated with increased risk of coronary heart disease, and postulated as a major genetic susceptibility locus for Alzheimer's disease. Studies undertaken in different populations have shown different association patterns between apo E genotype and stroke. The aim of this study was to determine the risk of apo E genotype in stroke patients living in the eastern part of Turkey. The apo E genotypes and allele frequencies of 229 individuals from the same geographic area were determined by polymerase chain reaction and restriction fragment length polymorphism, of which 103 were patients with a documented history of stroke without other apparent dementia and 126 age-matched healthy subjects as a control group. A reduced E3/4 genotype frequency was found in subjects with stroke and the E2/3 genotype frequency was elevated in patients with previous stroke. There was no association between apo E epsilon4 allele and stroke. The APOE alleles had divergent effects in this population. Association between APOE (the gene) alleles and stroke in this population may be altered due to interaction with other genetic effects. The effects of APOE alleles and genotypes require further study in different populations.

Aged↗

PubMedDate not supplied

Contribution of the histaminergic receptor subtypes to histamine-induced cerebellar granular neurotoxicity.

In the present study, we investigated the effects of histamine and its specific H(1), H(2) and H(3) receptor blockers in cerebellar granular cell culture derived from rat pups. Histamine was applied at 10(-9),10(-8), 10(-7),10(-6), and 10(-5) M for 16 h into the cultures and the highest dose was found to be the most toxic one. Pheniramine (H(1) receptor blocker), ranitidine (H(2) receptor blocker) and thioperamide (H(3) receptor blocker) were applied at 10(-8), 10(-7), 10(-6), 10(-5) M into the flasks prior to histamine in the second step of the experiments. Also, the effect of all of the blockers together at 10(-5) M concentrations was tested on the toxicity induced by 10(-5) M histamine. The H(3) receptor blocker, thioperamide (10(-6) M) was demonstrated to be most effective histamine toxicity blocker. Histamine H(2) blocker, ranitidine, was found to attenuate histamine neurotoxicity at all doses tested, its most effective dose being the highest dose. On the other hand, H(1) blocker, pheniramine, was able to reverse the effect of histamine at 10(-6) and 10(-5) M, but it was found ineffective when given at 10(-9) and 10(-8) M. Combined application of H(1), H(2), and H(3) receptor blockers at 10(-5) M concentrations, 45 min before histamine addition into the flasks at 10(-5) M, was able to reduce cell death score but it was not as effective as H(3) blocker, thioperamide.

Animals↗