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The objective of this experiment was to investigate the ameliorative effect of vitamin E (Vit E) on tissue damage caused by heat stress in the testes of broilers, and to correlate this effect with the secretion of the HSP-70 protein. In the study totally 30 broilers (breed Ross 308) were used. Animals were divided into three groups, including the control group. Group Control (C); these broilers (24 o C) were not administered with Vit E in the diet and not subjected to heat stress. Group Stress (S); these broilers not administered with Vit E in the diet but subjected to heat stress (34 o C). Group Stress +Vitamin E (Group S + vit E); broilers subjected to heat stress (34 o C) and administered with vitamin E. Histopathological examination demonstrated the presence of degenerative alterations in testes tissue of the group S. However, there has been seen diminishing the severity of degeneration in the group S+Vit E. While secretion of HSP-70 was determined in the testes of all groups in varying degree, the highest secretion level of HSP-70 was in the group C, the lowest secretion level of HSP-70 was in the group S. It is concluded that heat stress reduces the secretion of HSP-70 in testes of broilers, when vitamin E is administered, the secretion of HSP-70 increases again and reduces tissues damage. Keywords: Heat stress, Broiler, Testis, Vit E, HSP-70 Sıcaklık Stresine Maruz Bırakılan Broilerlerin Testislerinde Vit E' in HSP-70 Sekresyonu Üzerine Etkisi ÖzetBu çalışmanın amacı broilerlerin testislerinde ısı stresinin sebep olduğu doku hasarı üzerine vitamin E (Vit E)'in iyileştirici etkisini araştırmak ve bu etkinin HSP-70 proteininin sekresyonu ile ilişkisini ortaya koymaktır. Çalışmada toplam olarak 30 adet (Ross 308 ırkı) broiler kullanıldı. Hayvanlar kontrol grubu da dahil olmak üzere üç gruba ayrıldı. Grup kontrol (C); sıcaklık stresine maruz bırakılmayan (24 o C) ve diyetlerine Vit E eklenmeyen broiler. Grup stress (S); diyetlerine Vit E eklenmeyen ancak sıcaklık stresine maruz bırakılan (34 o C) broiler. Grup Stres +Vitamin E (Grup S + vit E); sıcaklık stresine maruz bırakılan (34 o C) ve diyetlerine vitamin E eklenen broiler. Histopatolojik inceleme S grubunun testislerinde dejeneratif değişiklikler gösterdi. Ancak S + Vit E grubunda dejenerasyonun şiddetinin azaldığı gözlendi. Grupların tamamının testislerinde farklı seviyede HSP-70 sekresyonu saptanırken, HSP-70'in en yüksek seviyesi grup C'de en düşük seviyesi grup S'deydi. Isı stresinin broilerlerin testislerinde HSP-70 sekresyonunu azaltığı, vitamin E uygulandığında, HSP-70 sekresyonunun yeniden artığı ve doku hasarını azalttığı sonucuna varıldı.

The aim of this study was to evaluate the possible therapeutic or protective effects of Helichrysum plicatum DC. subsp. plicatum ethanol extract (HPE) against gentamicin-induced nephrotoxicity. Thirty-six Sprague Dawley male rats weighing between 200 and 250 g were used as live material. They were formed into six groups containing 6 rats each and were allowed to adapt to laboratory conditions for 7 d. Group I: control, 5% DMSO intraperitoneal (i.p.); Group II: HPE 100 mg/(kg·d) i.p.; Group III: HPE 200 mg/(kg·d) i.p.; Group IV: gentamicin as 80 mg/(kg·d) i.p.; Group V: gentamicin as 80 mg/(kg·d) i.p.+HPE 100 mg/(kg·d) i.p.; and Group VI: gentamicin as 80 mg/(kg·d) i.p.+HPE 200 mg/(kg·d) i.p. for 8 d. Following treatment, serum, liver, and kidney tissues were used to assess blood urea nitrogen (BUN), creatinine, enzymatic and non-enzymatic antioxidants, and lipid peroxidation. Gentamicin significantly increased serum BUN, creatinin, and liver and kidney levels of malondialdehyde (MDA). It also decreased the activity of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD). Treatment with the HPE 100 mg/kg reversed gentamicin-induced alterations as evidenced by decreased serum BUN and creatinin, liver and kidney oxidant marker, and tubular necrosis as well as by an increase in antioxidant enzymes. It was found that HPE 200 mg/kg significantly increased liver and kidney tissue MDA levels in nephrotoxicity in rats. As a result, these findings support the proposition that HPE in 100 mg/kg dose demonstrates in the kidney and liver as free radicals and scavenger to prevent the toxic effects of gentamicin in both the biochemical and histopathology parameters.

Astaxanthin (ASX) is a xanthophyll family of hydroxycarotenoids which contains several double bonds. It is produced by Haemococcus pluvialis, a microalgae and possesses antioxidant and anti-inflammatory properties. The aim of this study was to test whether ASX could protect against oxidative damage in the testicular tissues of rats receiving high fructose. The rats (n = 24) were randomly divided into two main groups: control and fructose (30%, via drinking water) and then each main group either not supplemented or supplemented with ASX (1 mg kg day , within 0.2 ml olive oil) via oral gavage. Data were subjected to two-way ANOVA. High fructose consumption tended to increase testis weight and serum testosterone concentration and decreased testicular tissue glutathione-S-transferase (GST) and superoxide dismutase (SOD) levels, but did not affect testicular tissue malondialdehyde (MDA) concentration. Astaxanthin administration increased testosterone, GST and SOD levels and testis weight and decreased MDA concentration. However, ASX administration did not reverse alterations in antioxidant parameters caused by high fructose consumption. Inducible nitric oxide synthase (iNOS) tended to increase in sertoli cell, spermatid and spermatogonia, but not in spermatocytes and leydig cell in response to high fructose consumption. Astaxanthin administration tended to reverse elevation in iNOS in testis cells. In conclusion, ASX could help alleviate oxidative damage caused by high fructose consumption.

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