Is ceftriaxone effective in experimental brain ischemia/reperfusion injury?

OBJECTIVE: The aim of the present study was to investigate the neuroprotective effect of ceftriaxone in a rat brain ischemia/reperfusion injury model. METHODS: The oxidative stress parameter, malondialdehyde (MDA) levels with or without ceftriaxone treatment in brain ischemia/reperfusion injured rats as well as in controls were measured in serum and brain tissue. Motor examinations of the rats were also performed. One-way Analysis of Variance (ANOVA) test was used for analysis. Duncan's Multiple Range Test was performed in multiple comparisons. p < 0.05 were considered statistically significant.  RESULTS: The data of this study showed that ceftriaxone treatment reduced the MDA levels in brain tissues in ischemia/reperfusion injured rats. Moreover, Bederson motor scores were higher in the ceftriaxone treated group as compared to the ischemia group (p = 0.092). CONCLUSION: These results suggest that ceftriaxone could be beneficial for the prevention of brain ischemia/reperfusion injury caused by acute arterial occlusion through reducing the tissue MDA level (Tab. 2, Fig. 5, Ref. 24).

N-acetylcysteine protects testicular tissue against ischemia/reperfusion injury via inhibiting endoplasmic reticulum stress and apoptosis.

BACKGROUND: In animal models, endoplasmic reticulum (ER) stress has been reported to play a vital role in mediating ischemia/reperfusion (I/R) injury in certain organs, such as brain, liver, and intestine. However, there are a limited number of studies examining the relationship between ER stress and torsion and detorsion (T/D)-induced testicular injury. OBJECTIVE: To investigate the effects of N-acetylcysteine (NAC) on ER-stress and apoptosis in an experimental testicular I/R injury model. DESIGN: A non-blinded experimental study with three arms. Rats were divided into three groups: control group, T/D group, and NAC group. In the pretreatment of the NAC group, 20 mg/kg NAC was given intraperitoneally 30 min before detorsion. Tissue 4-hydroxynonenal (4-HNE), 78-kDa glucose-regulated protein (GRP78), and activating transcription factor 6 (ATF6) levels were determined using enzyme-linked immunosorbent assay. The apoptosis levels were evaluated using terminal deoxynucleotide transferase-mediated dUTP nick-end label assay. RESULTS: In T/D group, tissue 4-HNE, GRP78, ATF6, and apoptotic index levels were significantly higher than control group. These increases were significantly reversed with NAC pretreatment. DISCUSSION: There are some potential drugs that have been shown to reduce ER stress in the experimental ischemia model, and it is questioned that these drug candidates can be used as a therapeutic agent in the treatment of ischemic diseases in the near future. This study was not without limitations. First, the authors applied NAC only 20 mg/kg. In a future study, a dose-dependent assay should be performed to assess the likelihood of an additional testicular protective effect. One limitation of this research is also that in vivo studies cannot be extrapolated to possible effect in clinics. More experiments therefore need to be conducted to extrapolate the study findings to humans. CONCLUSION: The study results showed that, after testicular torsion (TT), the ER stress-related apoptotic pathway plays a pivotal role in testicular injury. Further studies of other experimental models of TT may prove that NAC is a useful agent as an adjunctive treatment in surgical repair in human cases.

Lasting hepatotoxic effects of prenatal mobile phone exposure.

OBJECTIVE: In this study, the livers of rats born to mothers exposed to electromagnetic field (EMF) were examined 60 days postpartum for biochemical and histopathological changes. METHODS: Pregnant rats were exposed to radiation (900 MHz EMF, 24 h/day for 20 days) using a digital signal generator by placing the device centrally under the cage, which formed the study (EMF) group, while untreated matching rats served as controls. Livers and blood were obtained from litters (seven males and seven females) of both groups 60 days after birth, which were used for biochemical and histopathological analyses. RESULTS: There was a significant increase in the levels of malondialdehyde (MDA) (p < 0.05) that was accompanied by a significant fall in glutathione (GSH) (p < 0.01) in the liver. The serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were significantly increased (p < 0.05). Histopathologically, the liver sections of the EMF group showed intense degeneration in hepatocytes with cytoplasmic eosinophilic structures, pyknotic nuclei and fibrosis. CONCLUSION: We demonstrate that the intrauterin harmful effects of EMF on the livers of rats persist into adulthood.

Borax partially prevents neurologic disability and oxidative stress in experimental spinal cord ischemia/reperfusion injury.

OBJECTIVES: The aim of this study is to investigate the potential effects of borax on ischemia/reperfusion injury of the rat spinal cord. METHODS: Twenty-one Wistar albino rats were divided into 3 groups: sham (no ischemia/reperfusion), ischemia/reperfusion, and borax (ischemia/reperfusion + borax); each group was consist of 7 animals. Infrarenal aortic cross clamp was applied for 30 minutes to generate spinal cord ischemia. Animals were evaluated functionally with the Basso, Beattie, and Bresnahan scoring system and inclined-plane test. The spinal cord tissue samples were harvested to analyze tissue concentrations of nitric oxide, nitric oxide synthase activity, xanthine oxidase activity, total antioxidant capacity, and total oxidant status and to perform histopathological examination. RESULTS: At the 72nd hour after ischemia, the borax group had significantly higher Basso, Beattie, and Bresnahan and inclined-plane scores than those of ischemia/reperfusion group. Histopathological examination of spinal cord tissues in borax group showed that treatment with borax significantly reduced the degree of spinal cord edema, inflammation, and tissue injury disclosed by light microscopy. Xanthine oxidase activity and total oxidant status levels of the ischemia/reperfusion group were significantly higher than those of the sham and borax groups (P < .05), and total antioxidant capacity levels of borax group were significantly higher than those of the ischemia/reperfusion group (P < .05). There was not a significantly difference between the sham and borax groups in terms of total antioxidant capacity levels (P > .05). The nitric oxide levels and nitric oxide synthase activity of all groups were similar (P > .05). CONCLUSIONS: Borax treatment seems to protect the spinal cord against injury in a rat ischemia/reperfusion model and improve neurological outcome.

Generalized aggressive periodontitis in a prepubertal patient: a case report.

A 10-year-old boy presented with generalized gingival inflammation, extensive alveolar bone loss, and tooth mobility. Clinical and radiographic examination supplemented by microbiologic investigation led to a diagnosis of classically termed prepubertal periodontitis (now known as generalized aggressive periodontitis). Other than severe periodontitis, the child was systemically healthy. Neither unusual infections nor abnormalities in neutrophil functions were detected. Microbiologic examinations by culture revealed the presence of the periodontal pathogen Actinobacillus actinomycetemcomitans. Treatment consisted of extraction of mobile teeth, supragingival and subgingival debridement, subgingival curettage, and root planing combined with a 1-week prescription of a combination of metronidazole and amoxicillin. Scanning electron microscopy of extracted teeth revealed hypoplastic and aplastic cementum at the periodontally exposed and intact surfaces. Clinical and microbiologic follow-up was continued over a 1-year period. No periodontal lesions have been detected, and A actinomycetemcomitans could not be isolated from the subgingival areas of the remaining teeth at the end of the first year. Since A actinomycetemcomitans was the main pathogen present in the subgingival microflora of the patient, it might play a key role in the etiology of prepubertal periodontitis.