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Major gingival-periodontal changes according to age have been observed in both diabetic and non-diabetic rats. Male Wistar rats weighing 200-220 g were divided into two groups: 1) Nondiabetic (ND) and 2) Diabetic (D) by receiving an intraperitoneal (ip) dose of streptozotocin (STZ) (50 mg /kg). Animals from both groups (ND and D) were euthanized at 4, 8, 12, 17 y 25 weeks after treatment with saline solution or STZ. Glycemia values in ND rats were 5 to 6 mmol/L, while in D, glycemia increased progressively between weeks 4 and 25, with values ranging from 18. 3±2. 1 to 39. 3±2. 7 mmol/L. Oxidative stress differed significantly in gums of ND and D rats. ND: lipid peroxidation: Malondialdehyde (MDA): 8. 52±1. 2 to 15. 5±2(nmol/mgP); superoxide dismutase (SOD): 37. 1±4. 2 to 21. 2±1. 3 (U/100mgP); D: MDA 13. 1±1. 6 to 22. 9±2. 7 (nmol/L); superoxide dismutase (SOD): 17. 7±0. 8 to 9. ±0. 2 (U/100mgP). Vascular permeability (VP) and gingival edema (E) showed significant changes between ND and D rats from 4 to 25 weeks. ND: PV: 10±0. 2 to 16. 1±1. 3 (EB ug/g dry t); E: 0. 9±0. 1 to 4. 1±1. 3 ml; D: PV: 12±1. 2 to 24. 4±1. 6 (EB ug/g dry t); E: 2. 2±0. 2 to 8. 4±1. 3 ml. Aging produced progressive natural changes in oxidative stress, VP and gingival E. In diabetic animals, changes in oxidative stress, VP and gingival E were observed early and were progressively more significant than for ND. According to these results, non-diabetic gingival modifications develop naturally with age, while in aging associated to diabetic disease, hyperglycemia increases progressively and early.Se han observados importantes cambios gingivo-periodontales en función de la edad tanto en ratas no diabéticas como en ratas diabéticas. Ratas machos Wistar de 200-220 g de peso corporal fueron separadas en dos grupos: 1) No diabéticas(ND) ; 2) Diabéticas (D), por haber recibido una dosis intraperitoneal (ip) de estreptozotocina (STZ) (50 mg íkg). Ambos grupos de ratas (ND y D) fueron sacrificados a las 4, 8, 12, 17 y 25 semanas de edad después del tratamiento con solución salina o con STZ. En ratas ND las los valores de glucemia fueron de 5 a 6 mmol/L, en tanto que en las D las glucemias se observaron progresivamente aumentadas entre las 4 y las 25 semanas con valores entre 18. 3±2. 1 a 39. 3±2. 7 mmol/L. El estrés oxidativo mostró diferencias significativas entre las encías de animales ND respecto a los D; ND: peroxidacion lipidica: Malondihaldeido (MDA): 8. 52±1. 2 a 15. 5±2(nmol/mgP);superoxido dismutasa (SOD):37. 1±4. 2 a 21. 2±1. 3 (U/100mgP); D : MDA 13. 1±1. 6 a 22. 9±2. 7 (nmol/L); Superoxidodismutasa :SOD 17. 7±0. 8 a 9. ±0. 2 (U/100mgP). La permeabilidad vascular(PV) y el edema(E) gingival mostraron cambios significativos entre las 4 y las 25 semanas de edad entre los animales ND respecto a los D : ND : PV: 10±0. 2 a 16. 1±1. 3 (EB ug/g t seco); E :0. 9±0. 1 a 4. 1±1. 3 ml; D: PV :12±1. 2 a 24. 4±1. 6 (EB ug/g t seco); E 2. 2_/- 0. 2 a 8. 4± 1. 3 ml. El envejecimiento produjo cambios progresivos naturales en el estrés oxidativo, PV y Egingival. En tanto que en el estado diabético los cambios del estrés oxidativo, PV y E gingival se observan temprano y fueron progresivamente más significativos comparados con los ND. De acuerdo a estos resultados las modificaciones gingivales no diabéticas se desarrollan naturalmente en función de la edad, en cambio en la senectud asociada con enfermedad diabética la hiperglucemia aumenta progresiva y tempranamente.

The purpose of the present work was to evaluate the kallikrein-kinin system and effects of hypothermia during renal ischemia and reperfusion. Male C57BL/KSJmdb mice were subjected to 20 or 60 min ischemia for different periods of reperfusion. Our results demonstrate that short periods of ischemia followed by reperfusion did not cause significant alterations in kallikrein activity, Evans Blue (EB) extravasation, prokallikreins, myeloperoxidase activity or plasma creatinine concentration. Edema was evident at 1 h reperfusion in the treated mice, but returned to basal values after 24 h reperfusion. Kallikrein activities and EB extravasation showed a significant increase in 60 min ischemic mice. Myeloperoxidase activity in the kidney of the mice confirmed net infiltration in the group with 60 min ischemia and 24 h reperfusion. The generation of kinins and activation of matrix degrading enzymes by tissue kallikrein, liberated from both renal and infiltrated leukocytes, could be responsible at least in part for the damage observed in the kidney of mice subject to 60 min ischemia and reperfusion. The hypothermia significantly reduced the inflammatory process in the 60 min ischemic mice, and did prevent an increase in vascular permeability. Nevertheless, the tissue edema was not shown to change between normothermic and hypothermic ischemic mice.

Sub-diabetogenic doses of streptozotocin (STZ) produce insulitis, β cell destruction and diabetes in mice. Since kinin have been proposed as an inflammatory mediator in several diseases, we decided to evaluate the role of the kallikrein–kinin system in the evolution of insulitis. Male C 57 BL/KsJ mdb mice were injected with STZ (40 mg/kg) for 5 consecutive d. Aprotinin (4000 KIU/d) was injected simultaneously with STZ during 10 d. Plasma and urine samples collected on day 15 were assayed for glucose concentration and proteins, nitrites and kallikrein. Diabetic mice showed hyperglycemia and increased diuresis, marked proteinuria, nitrites and kallikrein. Administration of aprotinin, a potent tissue kallikrein inhibitor, to STZ mice, reduced the hyperglycemia and the altered renal function of the diabetic mice to level no different from normal mice. The present studies are consistent with the hypothesis that the over-production of tissue kallikrein in insulitis could be controlled by the effect of aprotinin.

Gingival overgrowth is an adverse side effect of cyclosporine A (CsA) in the treatment of transplanted patients. The purpose of this study was to evaluate the effects of CsA on new-onset diabetes mellitus and gingival overgrowth in rats, by measuring collagen, nitric oxide and microvascular permeability. Blood glucose level, collagen, nitric oxide level and vascular permeability were determined. Blood glucose level increased significantly from 6.5 +/- 0.9 for the control group to 15 +/- 1.2, 17 +/- 1.2 and 21.6 +/- 1.6 mM/L at 1, 4 or 8 weeks of CsA treatment, respectively. Collagen (ug HO Proline/mg p) increased significantly from 2.5 +/- 0.5 for the control group to 4.2 +/- 0.8, 5.9 +/- 0.6 and 7.3 +/- 0.8 at 1, 4 or 8 weeks of CsA treatment, respectively. Vascular permeability was 10.3 +/- 1.2 for the control group and 15 +/- 1; 17.2 +/- 1.3, and 22.1 +/- 2.1 ug EB/g T; at 1, 4 or 8 weeks of CsA treatment, respectively Nitric oxide level was 3.5 +/- .9 umol/mg P for the control group and 4 +/- 0.2, 8.2 +/- 0.9 and 11 +/- 1 for 1, 2 or 8 weeks of CsA treatment, respectively. These findings appear to indicate that the development of significant gingival changes induced by CsA is related to new-onset of diabetes mellitus during the immunosuppressive treatment.

Data derived from animals and humans suggest that the onset of diabetes is associated with hemodynamic changes in the renal circulation leading to increased renal plasma flow (RPF), glomerular capillary hyperfusion, and an increased glomerular transcapillary hydraulic pressure gradient. The duration of diabetes is one of the most important factors in predicting the development of diabetic nephropathy. On the other hand, diabetic nephropathy has been associated with the degree of hyperglycemia; thus, hyperglycemia may therefore contribute to alterations in structure and function of the kidney. In the present paper, we investigated early alterations of renal function in C57BL/KSJ mdb male mice that were injected with sub-diabetogenic doses of STZ. Urinary protein excretion (UPE) increased significantly at 12 and 18–20 days after STZ with a glucose level of 4–6 mm/l; the progressive increase of glycemia was followed by a progressive increase of UPE. In a similar way, urinary nitrite (NO2−) was also significantly increased. Urinary kallikrein excretion started to increase at a level of 4–6 mmol/l blood glucose concentration (BGC) 8 days after administration of STZ, and kidney vascular permeability also increased following the increment of BGC. These results confirm the presence of early modifications of renal function prior to the clinical detection of diabetic hyperglycemia.

Kallikrein/kinin system; Diabetes Insulitis is an inflammatory state of the islet of Langerhans (Catanzaro et al., 1994). The inflamma- tory process is sustained by synthesis and release of a large number of humoral mediators, that, in turn, initiate a cascade of systemic and local effector molecules. Kinins have long been proposed as prominent inflammatory mediators in the pathogene- sis of several diseases (Sharma and Moshin, 1990; Sharma, 1991), because they can induce all the cardinal signs of inflammatory reactions. The present study was designed to evaluate the mechanisms of the endogenous kinins in the evolution of insulitis. Male C57BL/Ks mdb mice were injected with strep- tozotocin (STZ) for 5 consecutive days (40 mg/kg

The submandibular gland of cri/cri and control mice were compared for their activity of glandular kallikrein like esteroprotease and kininase. Esteroprotease activity is significantly reduced in cri/cri mice with respect to control, with an increased kininase activity in cri/cri mice. Since previous work showed an electrolyte abnormality in the salivary glands of this mutant mouse (1) a possible relationship between this alteration with the low activity of cellular esteroprotease and the high kininase activity is suggested.

In the salivary glands TsTx can stimulate a number of receptor mechanism(s) including cholinergic, β-adrenergic, α-adrenergic and probably substance P., (Catanzaro, et al., 1976).