ABSTRACT
BACKGROUND: When diagnosing and treating male infertility it is important to determine whether there are defects in the maturation process of sperm nuclei. Using nutritional supplements can improve the morphological and physiological condition of the spermatozoa. In recent years there has been an increase in the usage of supplements with different compositions which strives to determine the best combination and avoid side effects. AIM: To study the effect of PAPA nutritional supplement on the levels of DNA fragmentation of sperm cells tested with acridine orange test (single stranded DNA against double stranded DNA) in men with sub/infertility. MATERIALS AND METHODS: 48 men with confirmed sub/infertility underwent treatment for three months with nutritional supplement PAPA containing 9 micronutrients. The differences in levels of DNA fragmentation were determined with acridine orange test, which was conducted before and after the treatment. RESULTS: The results were statistically significant (p<0.001) showing an increase in the number of green spermatozoa (normal DNA), and a decrease of damaged ones (orange and red). After treatment the level of sperm DNA fragmentation decreased by 10.2%. CONCLUSION: Men with confirmed sub/infertility that took nutritional supplement PAPA for three moths showed a decrease in DNA fragmentation levels of 10.2% determined by AO test which implies an improvement of male fertility levels.
Subject(s)
DNA Fragmentation , Dietary Supplements , Infertility, Male/therapy , Spermatozoa/metabolism , Acridine Orange , Adult , Antioxidants/therapeutic use , Arginine/therapeutic use , Asthenozoospermia/therapy , Carnitine/therapeutic use , Fluorescent Dyes , Folic Acid/therapeutic use , Fructose/therapeutic use , Glutathione Reductase/therapeutic use , Humans , Male , Middle Aged , Oligospermia/therapy , Selenium/therapeutic use , Sweetening Agents/therapeutic use , Taurine/therapeutic use , Ubiquinone/analogs & derivatives , Ubiquinone/therapeutic use , Vitamin E/therapeutic use , Vitamins/therapeutic useABSTRACT
Hydrogen sulfide (H(2)S) is a new gasotransmitter synthesized enzymatically from l-cysteine in cytosol and is oxidized in mitochondria. In the cardiovascular system, H(2)S regulates vascular tone, inhibits atherogenesis, and protects against myocardial ischemia-reperfusion injury. We examined the effect of statins on vascular H(2)S production. Male Wistar rats received pravastatin (40mg/kg/day) or atorvastatin (20mg/kg/day) for 3 weeks and then H(2)S formation was measured in aortic media, periaortic adipose tissue (PAAT) and the liver. Only atorvastatin increased H(2)S production in PAAT whereas both statins stimulated its formation in the liver. Neither statin affected H(2)S production in aortic media. H(2)S formation in post-mitochondrial supernatant was higher than in mitochondria-containing supernatant and was not influenced by statins in any tissue. In addition, oxidation of exogenous H(2)S in isolated liver mitochondria was slower in statin-treated than in control rats. These data indicate that statins increase net H(2)S production by inhibiting its mitochondrial oxidation. Statins had no effect on the activity of H(2)S-metabolizing enzyme, sulfide:quinone oxidoreductase, measured at saturating coenzyme Q concentration. Both statins reduced CoQ(9) concentration in plasma and liver, but only atorvastatin decreased CoQ(9) in PAAT. Atorvastatin attenuated phenylephrine-induced contraction of PAAT+ but not of PAAT- aortic rings. Effects of atorvastatin on net H(2)S production, mitochondrial H(2)S oxidation and aortic contractility were abolished by supplementation of exogenous CoQ(9). In conclusion, lipophilic atorvastatin, but not hydrophilic pravastatin, increases net H(2)S production in perivascular adipose tissue by inhibiting its mitochondrial oxidation. This effect is mediated by statin-induced CoQ(9) deficiency and results in the augmentation of anticontractile effect of perivascular adipose tissue.
Subject(s)
Adipose Tissue/drug effects , Aorta, Thoracic/drug effects , Heptanoic Acids/pharmacology , Hydrogen Sulfide/metabolism , Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology , Pravastatin/pharmacology , Pyrroles/pharmacology , Vasodilation/drug effects , Adipose Tissue/metabolism , Animals , Aorta, Thoracic/metabolism , Atorvastatin , Cholesterol/blood , Cholesterol, HDL/blood , Dose-Response Relationship, Drug , KATP Channels/drug effects , KATP Channels/metabolism , Liver/drug effects , Liver/metabolism , Male , Mitochondria, Liver/drug effects , Mitochondria, Liver/metabolism , Oxidation-Reduction , Potassium Channel Blockers/pharmacology , Quinone Reductases/metabolism , Rats , Rats, Wistar , Sulfides/metabolism , Triglycerides/blood , Ubiquinone/analogs & derivatives , Ubiquinone/metabolism , Vasoconstrictor Agents/pharmacologyABSTRACT
UNLABELLED: The aim of the present experimental study was to follow up the connective tissue response after using ProRoot MTA and Titan cement to repair furcation perforations in dogs. MATERIAL AND METHODS: Four animals aged 12 to 18 months were used in the study. Perforation defects were created in the center of the pulp chamber of mandibular premolars P2, P3 and P4, right and left. The defects on the left side were repaired with ProRoot MTA, and those on the right side--with Titan cement in all dogs. After 30 days bone fragments with teeth included were fixed in formalin and decalcified in 50% formic acid. Serial sections of 10 microm thickness were prepared, stained with hematoxylin and eosin and studied under light microscopy. RESULTS: The connective tissue response in the Titan cement repaired teeth was a fibrous capsule in contact with the material, with single or aggregated lymphocytes seen in the vicinity. The response to ProRoot MTA was similar, but the fibrous capsule was thinner and without any aggregation of lymphocytes. CONCLUSIONS: The connective tissue response was similar for both tested materials. The tissues tolerated both of them well; it formed a fibrous capsule, which is indicative of the start of a healing process.
