ABSTRACT
Nonylphenol (NP) is an organic pollutant and endocrine disruptor chemical that has harmful effects on the environment and living organisms. This study looked at whether kidney tissues subjected to increasing doses of nonylphenol generated alterations in histopathologic, pro-inflammatory, and autophagic markers. Fifty rats were divided into five groups of ten each: group I: healthy group, II: control (corn oil), group III: 25 µl/kg NP, group IV: 50 µl/kg NP, group V: 75 µl/kg NP. The kidney tissue samples were obtained for histopathological, immunohistochemical, and biochemical analyses. The histological deteriorations observed in all NP groups included tubular epithelial cell degeneration, inflammation areas, and hemorrhage. The immunohistochemical investigations showed that NP significantly elevated the autophagy markers (Beclin-1, LC3/2, p62), pro-inflammatory cytokines (TNF-α, IL-6), HIF-1α, and eNOS in group III, IV and V compared with group I and II. The biochemical analysis also revealed that pro-inflammatory cytokines (TNF-α, IL-1ß, and IL-6) increased in correlation with the NP doses, but only IL-1ß reached statistical significance in NP treated rats kidney tissue. The biochemical findings have been confirmed by the histological studies. The damage to renal tissue caused by NP exposure may worsen it by increasing inflammatory and autophagic markers.
ABSTRACT
Ovarian ischemia is a gynecological emergency that occurs as a result of ovarian torsion, affects women of reproductive age, and reduces ovarian reserve. The current study was designed to investigate the effect of boric acid taken in different ways on histopathological changes, autophagy, oxidative stress, and DNA damage caused by ischemia and reperfusion in the ovary of adult female rats. We established seven groups of 70 adult female rats: untreated control, intraperitoneal boric acid group (IpBA), oral boric acid group (OBA), ischemia/reperfusion group (ischemia/2 h reperfusion; OIR), ischemia/reperfusion and local boric acid group (OIR + LBA), ischemia/reperfusion and intraperitoneal boric acid group (OIR + IpBA), and ischemia/reperfusion and oral boric acid group (OIR + OBA). On the 31st day of the experimental procedure, both ovaries were harvested for histologic (hematoxylen and eosin and Masson trichrom), biochemical (ELISA and AMH, MDA, SOD, and CAT analyses), and comet evaluation. In the OIR group, hemorrhage, edema, inflammation, and diminished follicle reserve were seen in the ovary. Boric acid treatment reduced the ovarian ischemia/reperfusion damage, and the follicles exhibited similar morphological features to the control group. Moreover, boric acid treatment decreased the levels of Hsp70, NF-KB, COX-2, and CD31, which increased as a result of OIR. On the other hand, SCF and AMH levels, which decreased as a result of OIR, increased with boric acid treatment. The levels of autophagy markers (Beclin-1, LC3, and p62) reached values close to those of the control group. According to the biochemical findings, it was concluded that boric acid is also effective on oxidative stress, and the AMH level was particularly high in the OIR + OBA group, consistent with the immunohistochemical staining result. In addition, it was observed that the DNA damage caused by OIR reached values close to those of the control group, especially in the OBA after OIR. This study showed the therapeutic effects of boric acid on OIR injuries; thus, boric acid may be a potential therapeutic agent for ovarian protection and fertility preservation in cases that may cause ovarian torsion.
