Glucose as a Risk Factor for Periodontitis in Kidney Transplantation Patients.

BACKGROUND: Various factors including diabetes and oxidative stress are associated with periodontal inflammation. End-stage renal disease causes various systemic abnormalities in patients, including cardiovascular disaese, metabolic abnormalities, and infection. Even after kidney transplantation (KT), these factors are known to be associated with inflammation. Our study, therefore, aimed to study risk factors associated with periodontitis in KT patients. METHODS: Patients who visited Dongsan Hospital, Daegu, Korea since 2018 and have undergone KT were selected. As of November 2021, 923 participants, with full data including hematologic factors were studied. Periodontitis was diagnosed based on residual bone level in panoramic views. Patients were studied by the presence of periodontitis. RESULTS: From 923 KT patients, 30 were diagnosed with periodontal disease. Fasting glucose levels were higher in patients with periodontal disease, and total bilirubin levels were lower. When divided by fasting glucose levels, high glucose level showed increase of periodontal disease with odds ratio of 1.031 (95% confidence interval 1.004-1.060). After adjusting for confounders, the results were significant with odds ratio of 1.032 (95% CI 1.004-1.061). CONCLUSIONS: Our study showed that KT patients, of whom uremic toxin clearance has been revolted, are yet at risk of periodontitis by other factors, such as high blood glucose levels.

Cyclosporine-induced apoptosis in osteosarcoma cells.

INTRODUCTION: Posttransplant bone disease is one of the complications of cyclosporine (CsA), which is widely used as an immunosuppressive agent in the field of kidney transplantation. Cyclosporine treatment causes osteopenia as a result of altered bone turnover, but the pathogenic mechanisms of this process remain unclear. This study examined the ability of CsA to induce apoptosis in a rat osteoblast cell line. RESULTS: We induced apoptosis in rat osteoblastic ROS 17/2.8 cells by exposure to CsA. MTT assay showed that CsA exhibited significant cytotoxic effects on ROS 17/2.8 cells in a dose-dependent manner. Western blot analysis showed enhanced processing of caspase-8, Bax, and p53 after CsA treatment. Expression of cleaved poly (ADP-ribose) polymerase (PARP) was elevated by CsA treatment. Pro-caspase-3 and Bcl-2 proteins were decreased by CsA. CONCLUSIONS: These results suggested that CsA induced apoptosis of osteoblasts.

Effect of vasoactive intestinal peptide and acetylcholine on penile erection in the rat in vivo.

We investigated the effect of vasoactive intestinal peptide (VIP) and its combination with acetylcholine (ACh) on the erectile response in 52 adults rats. Intracavernous injection of VIP (10(-8) to 10(-5)M, ACh (10(-9) to 10(-5), or a combination of VIP (10(-7) to 10(-5) with ACh (10(-6 M) additively enhanced that erection but did not lead to a full erection. VIP-antagonist (10(-9) to 10(-5 M), as well as atropine alone (10 (-7) to 10(-5 M), partially suppressed full erection induced by cavernous nerve stimulation (1 Hz, 3-6 V) in a dose-dependent manner, and the combination of VIP-antagonist (10(-9) to 10(-5 M) with atropine (10(-6 M) showed an additive effect. The results indicate that although VIP as well as ACh in involved in penile erection, they are not likely to be principal neurotransmitters. Their clinical application in the treatment of impotence may be confined to use in conjunction with another vasoactive agent.

Role of nitric oxide in penile erection.

The present study was undertaken to investigate the role of nitric oxide (NO) in erectile physiology by correlating its action with the existence and activity of nitric oxide synthase (NOS), which produces NO. We applied Western blot analysis in both human and rat penile tissue. In the rat, reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase staining and spectrophotometric assay were also performed, in addition to in vivo electroerection study with pharmacological manipulation. Western blot analysis identified a protein of 155 KDa identical to the neural form of NOS in the human and rat penis. The NOS blot densities in the two species were similar, and both were lower than that in the rat cerebellum. Histochemical staining localized NOS to neurons innervating the corpora cavernosa, including the pelvic plexus, the cavernosal nerves and their terminal fibers within the corporeal erectile tissue, and dorsal penile nerves. NOS activity was also found in the cerebellum, urethra, penis, and urinary bladder, in decreasing order of intensity. Intracavernous injections of NOS inhibitor (L-NOARG or L-NAME in concentrations from 10(-6) M to 10(-3) M suppressed electrostimulation-induced erection in a concentration-dependent manner. Subsequent intracavernous injection of L-Arginine (10(-2) M) partially restored the erection. The neural form of constitutive NOS in the corpora cavernosa synthesizes NO, which mediates penile erection. Determination of cavernosal NOS expression or activity may permit characterization of certain pathological conditions that cause impotence.

Effects of cyclosporine on the antioxidant status and oxidative stress in the glioma cells.

OBJECTIVES: After organ transplantation, some patients suffer neurological complications. Among the immunosuppressants, cyclosporine can cause neurological side effects. However, the mechanisms of encephalopathy by cyclosporine are not fully understood. We measured the antioxidant status, the hydrogen peroxide level, and the malondialdehyde level in glioma cells after cyclosporine treatment. METHODS: The production of hydrogen peroxide was determined using a modified xylenol orange method. The amount of malondialdehyde was measured using the thiobarbituric acid assay. Total antioxidant status was measured using Free Radical Analytical System 4 with kits. RESULTS: Cyclosporine resulted in the production of hydrogen peroxide by the glioma cells. The increased production of hydrogen peroxide depended on the drug concentration. The antioxidant status was decreased in the glioma cells after cyclosporine treatment. The malondialdehyde level was not changed in glioma cells after cyclosporine treatment. CONCLUSIONS: Increased production of reactive oxygen species and decreased antioxidant status by cyclosporine in glioma cells may contribute to neurological side effects in transplantation patients.