ß-Glucan ameliorates cisplatin-induced oxidative and histological damage in kidney and liver of rats.

We investigated the effects of ß-glucan (ßg) on kidney and liver damage caused by cisplatin (CP), an antineoplastic agent widely used to treat many types of cancer, in a rat model. The side effects of CP in many tissues and organs limit its usage. ßg is a natural polysaccharide that is an effective free radical scavenger. A total of 28 rats were randomly divided into four groups. Group 1 was a non-intervention control, only feed and water were given. Group 2 was administered 7 mg/kg CP in a single dose. Group 3 was administered 50 mg/kg ßg orally for 14 days. Group 4 was administered ßg for 14 days, following a single dose of CP. At the end of the experiment, kidney and liver tissues were evaluated biochemically and histopathologically. Increased thiobarbituric acid-reactive substances (TBARS) levels, as well as decreased catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) activities, and reduced glutathione (GSH) levels, as well as histological damage, were noted in both the kidney and liver tissues of the CP group. However, ßg treatment prevented the oxidative and histopathological effects of CP. The study demonstrates the protective efficacy of ßg against CP-induced kidney and liver damage through the effect of its antioxidant properties.

Investigation into the protective effects of Naringenin in phthalates-induced reproductive damage.

OBJECTIVE: Di-n-butyl phthalate (DBP) is a ubiquitous environmental pollutant, extensively used as a plasticizer in many products, including plastics, cosmetics, and medical devices. Naringenin (NAR) is a flavonoid belonging to the flavanones subclass. It is widely distributed in several citrus fruits, bergamot, tomatoes, and other fruits. It is also found in its glycoside form (mainly naringin). Several biological activities have been ascribed to this phytochemical: antioxidant, antitumor, antiviral, antibacterial, anti-inflammatory, antiadipogenic, and cardioprotective effects. This study hypothesized that phthalates' possible reproductive damage mechanism is oxidative attack, and naringenin could have a protective effect against radical forms in the body through its antioxidant properties. MATERIALS AND METHODS: Thirty-two male rats were used in our study (n=8 each). Rats were randomly divided into four groups: Control, DBP, DBP +NAR and NAR. Phthalate (DBP) and NAR were administered through gastric oral gavage (phthalate group 500 mg/kg/day DBP; NAR group 50 mg/kg/day NAR). At the end of four weeks, testis tissue samples were taken under anesthesia. Testis tissue and blood samples were collected from the four groups in this study. Histological, biochemical and spermatological analyses were conducted. RESULTS: Tissue samples from the control and NAR groups showed normal histological appearance on light microscopy. The DBP group exhibited deterioration in seminiferous tubules, vascular congestion in capsule, vascular congestion between the seminiferous tubules, edema in the intestinal area and vacuolization, arrested spermatocytes in different stages of division; sloughing of cells into the seminiferous tubular lumen was observed. It was also observed that NAR treatment significantly inhibited and prevented the histopathological damage caused by DBP. Tissue TBARS, antioxidant parameters, sperm motility, sperm density and abnormal spermatozoon ratios were determined. As a result, it was shown that DBP caused oxidative damage by increasing TBARS levels and decreasing antioxidant parameters, increased abnormal sperm rate and decreased sperm motility, and concentration and histopathological damage, so the antioxidant activity of naringenin inhibited this damage. CONCLUSIONS: DBP had toxic effects in rat testis tissue; NAR treatment ameliorated these effects. Further studies are warranted to confirm our findings.

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.