Protective effects of salusin-α and salusin-ß on renal ischemia/reperfusion damage and their levels in ischemic acute renal failure.

Salusin-α and salusin-ß are expressed in many tissues including the central nervous system, vessels and kidneys; they have been shown to decrease endoplasmic reticulum stress during heart ischemia/reperfusion (I/R) and to decrease apoptosis. We investigated the relation of salusin-α and salusin-ß levels to acute ischemic renal failure. We also investigated whether these peptides are protective against renal I/R damage. Fifty-three rats were divided into six groups: control, I/R, I/R + salusin-α1, I/R + salusin-α10, I/R + salusin-ß1 and I/R + salusin-ß10. After removing the right kidney, the left kidney was subjected to ischemia for 1 h and reperfusion for 23 h. The treatment groups were injected subcutaneously at the beginning of ischemia with 1 or 10 µg/kg salusin-α, and 1 or 10 µg/kg salusin-ß. Histopathology was assessed at the end of the experiment. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX) activity and malondialdehyde (MDA) levels were measured in the kidney tissue. Serum levels of blood urea nitrogen (BUN), creatinine (Cre), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and interleukin-1 beta (IL-1ß) also were measured. Levels of salusin-α and salusin-ß were measured in the serum and kidney tissues of the control and I/R groups. SOD, CAT and GSH-PX activities were decreased and the levels of MDA, TNF-α, IL-6, IL-1ß, BUN and Cre were increased in the I/R group compared to controls. Severe glomerular and tubular damage was apparent in the I/R group compared to controls. The level of salusin-ß was decreased in the serum and kidney tissue of the I/R group compared to controls, whereas the level of salusin-α was decreased in the serum and increased in the kidney tissue. Salusin-α and salusin-ß administration increased SOD and GSH-PX enzyme activation and decreased the levels of MDA, TNF-α, IL-6 and IL-1ß compared to the I/R group. BUN and Cre levels were decreased in the I/R + salusin-α1 group and the level of Cre was decreased in I/R + salusin-ß10 group compared to the I/R group. We demonstrated a protective effect of salusin-α and salusin-ß against renal I/R damage. Changes in the levels of salusin-α and salusin-ß in the I/R group suggest that these peptides may be associated with acute renal failure.

Effects of training period on haemorheological variables in regularly trained footballers.

OBJECTIVE: To investigate the effects of one football training period on haemorheological variables in regularly trained footballers. METHOD: Ten subjects were randomly selected from the reserve team of a football club in the Turkish Premier League. During the last week of the football season, one day before a standard training session and two days after the previous league match, venous blood samples were taken (pre-exercise). After 90 minutes of standard training, further blood samples were taken (post-exercise). Blood lactate, blood viscosity, plasma fibrinogen, blood clotting time, acid-base variables, and plasma Na+, K+, and Ca2+ were determined. RESULTS: Haemoglobin, packed cell volume, and mean corpuscular volume were all significantly decreased, whereas white blood cells and platelets were both increased after training. Blood viscosity decreased but the reduction was not significant. Blood lactate, plasma glucose, and Na+ content were significantly increased, but standard bicarbonate, actual bicarbonate, and Ca2+ were significantly decreased. Blood clotting time had shortened significantly after training. Blood viscosity was inversely correlated with plasma glucose concentration (r = -0.48 and p = 0.032). CONCLUSIONS: The results show that blood viscosity tends to decrease as the result of this type of training. This is due to a reduction in packed cell volume and mean corpuscular volume. The increased blood lactate does not have an adverse effect on the blood viscosity of these subjects because protective mechanisms develop with regular training throughout the season.

Neutrophil superoxide anion production, and CAT and GSSGR activity in patients with tuberculosis.

Tuberculosis (TB) is a chronic infection disease caused by Mycobacterium tuberculosis (MTB), as an intracellular pathogen. Various cytokines (TNF-alpha, IL's, GSF etc.) and other factors play important preventing roles and are secreted during the infection. It may cause changes in the metabolism of neutrophils. Production of superoxide anion and antioxidative enzymes activities, such as glutathione reductase (GSSGR) and catalase (CAT) may be changed during MTB infection in the host. In this study, the control group consisted of ten healthy subjects and ten patients with TB were studied before anti-TB treatment. Level of superoxide anion production, activity of CAT and activity of GSSGR were studied from peripheral neutrophils of healthy subjects and patients with TB. Catalase activities of the neutrophils were significantly lower in patients with TB than normal subjects (p < 0.01). Glutathione reductase activities of the neutrophils were also significantly lower in patients with TB than normal subjects (p < 0.05). Superoxide anion production in the neutrophils did not show any significant difference between TB and normal subjects (p > 0.05). As a result, the activities of CAT and GSSGR were lower in the peripheral neutrophils of patients with TB than normal subjects, whereas superoxide anion production in the neutrophils did not differ between in TB patients than normal subjects.