The role of deferoxamine in the prevention of gentamicin ototoxicity: a histological and audiological study in guinea pigs

Mostafa, Badr Eldin; Tawfik, Somia; Hefnawi, Nadia Galal El; Hassan, Mohammed Amir; Ismail, Fouad Abbas

doi:10.1080/00016480600794495

Cited by 25 publications

(17 citation statements)

References 12 publications

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“…Desferrioxamine, an iron chelating agent, was shown to be partially effective in gentamicin induced ototoxicity, through audiological and histopathological studies, by disrupting aminoglycoside-iron complexes [17] . Other iron chelating substances, such as dihydrochlorobenzoate and salicylates, also have antioxidant properties and have also been reported to be protective against amikacin toxicity [18] .…”

Section: Discussionmentioning

confidence: 99%

A Prospective Experimental Study on the Protective Effect of Resveratrol against Amikacin-Induced Ototoxicity in Rats

Avcı¹,

Erkan²,

Sönmez³

et al. 2016

Int Adv Otol

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OBJECTIVE:The purpose of this study was to evaluate the protective effect of resveratrol against amikacin-induced ototoxicity in rats by otoacoustic emission and histopathology of the cochlea. MATERIALS and METHODS:This study was conducted with 31 Sprague Dawley adult female rats that were 20-21 weeks old and 190-245 g in weight. Before the drug administration, distortion product otoacoustic emission (DPOAE) tests were performed in both ears of each rat. The rats were divided into four groups. Group 1 (n=7) received ethanol 1cc 4%, Group 2 (n=8) received 600 mg/kg amikacin, Group 3 (n=8) received 10 mg/kg resveratrol and 600 mg/kg amikacin, and Group 4 (n=8) received 1cc resveratrol at 10 mg/kg. The drugs were administered once a day for 21 consecutive days. Control DPOAE tests were performed at the 7 th , 14 th , and 21 st days after the administration of drugs. At the end of the study, the rats were sacrificed and their cochleae were dissected. The cochleae were evaluated for histopathologic changes. RESULTS:There was no statistically significant difference in the DPOAE measurements before the procedure between groups. The DPOAE measurements significantly decreased after the procedure in the amikacin group. There was no statistically significant difference in DPOAE measurements after the procedure in the amikacin + resveratrol, resveratrol, and ethanol groups. The histopathologic findings supported these results. CONCLUSION:We found that if resveratrol is administered with amikacin, the severity of amikacin-induced hearing loss is decreased. These findings suggest that resveratrol, a strong antioxidant, has a protective effect in amikacin ototoxicity.

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Section: Discussionmentioning

confidence: 99%

A Prospective Experimental Study on the Protective Effect of Resveratrol against Amikacin-Induced Ototoxicity in Rats

Avcı¹,

Erkan²,

Sönmez³

et al. 2016

Int Adv Otol

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“…Although GS is a very effective antibiotic, its use is often limited owing to its toxicity to non-target tissues (Aust, 2001). It is now well known that GS is severely ototoxic, but its effects are severe on vestibular functions rather than that of the cochlea (Reynolds, 1993), and ototoxicity seems to be due to oxidative stress (Feldman et al, 2007), which could be counteracted by a number of antioxidants (Mostafa et al, 2007). Reversible nephrotoxicity is a dose-limiting adverse effect of GS, which generally leads to acute renal failure (Al-Majed et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

An aminoglycoside antibiotic gentamycin induces oxidative stress, reduces antioxidant reserve and impairs spermatogenesis in rats

Narayana

2008

J. Toxicol. Sci.

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-Gentamycin (GS) is an aminoglycoside antibiotic used to treat infections of various Gram-negative organisms. The present study was designed to investigate the effects of GS on oxidative stress, antioxidant levels, testicular structure and sperm parameters in the rat. Adult Wistar rats (12 week old; N=7/group) were treated (i. p.) with 0 mg/kg, 3 mg/kg and 5 mg/kg for 10 days at an interval of 24 hr between subsequent treatments. Animals were sacrificed on days 1 and 35 after the last treatment, and the reproductive organs were removed and weights of testis and seminal vesicle were recorded. The right testis was processed for light microscopic analysis. The left testis was homogenized and step 19 spermatids were counted to determine the daily sperm production (DSP) and daily abnormal sperm production (DASP). The sperm count, sperm motility and incidence of abnormal sperms were estimated in the epididymis. In testicular sections, along with the evaluation of qualitative changes, the seminiferous tubule diameter (STD) and the epithelial height (SE) were measured. The incidence of stage XIV tubules in testicular sections, meiotic figures and step 14 spermatids/stage XIV tubule, and step 19 spermatids/stage VII tubule were estimated. Intra-testicular levels of superoxide anion, lipid peroxidation and antioxidantssuperoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and ascorbic acid were measured. GS did not affect the body weight, but the testis weight and DSP were decreased at 5 mg/kg dose-level on both days (p<0.05), and the weight of seminal vesicle decreased on day 35 at both dose-levels. The DASP was increased in a dose-dependent manner (p<0.05) on days 1 and 35 at both dose-levels. The sperm count was decreased at both dose-levels on day 35, whereas the sperm motility was decreased and sperm abnormality was increased on day 1 at 5 mg/kg and on day 35 at both dose-levels. GS induced structural changes such as sloughing of seminiferous epithelium, vacuoles and gaps in the epithelium, nuclear pyknosis and atrophic changes in a few tubules. The tubular shrinkage was observed as indicated by decreased STD and SE on both days at 5 mg/kg dose-level. Incidence of stage XIV tubules and step 19 spermatids/stage VII tubule decreased on all time points at all dose-levels, whereas the step 14 spermatids and meiotic figures decreased on day 35 at both dose-levels (p<0.05). The free radical-superoxide anion concentration was significantly increased on day 1 in a dose-dependent pattern (p<0.05). However, activities of all 3 enzymatic antioxidants and ascorbic acid level decreased in a dose-dependent pattern on day 1 (p<0.05), except the GPx, which was also decreased on day 35 at 5 mg/kg dose-level. There was a significant rise in the thiobarbituric acid reactive substances on day 1 indicating increased lipid peroxidation in the testis. In conclusion, GS induces an oxidative stress-status in the testis by increasing free radical formation and lipid peroxidation, and by decreasing the antioxidant reserves...

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“…Different aspects of ototoxicity and preventive agents have been previously studied [1][2][3][4][5][6][7][8][9] .…”

Section: Discussionmentioning

confidence: 99%

“…There are a few agents, including deferoxamine, 2.3-dihydroxybenzoate, steroids, α-tocopherol, α-lipoic acid, salicylates, trimetazadine, thymoquinone, mannitol, β-carotene, vitamins C and E, and magnesium [5][6][7][8][9][10][11][12][13][14] , that claim to prevent gentamicin ototoxicity. NAC also was shown to protect the sensory cells of the cochlea in a culture medium from the ototoxic effect of gentamicin [15] .…”

Section: Introductionmentioning

confidence: 99%

N-acetylcysteine Prevents Gentamicin Ototoxicity in a Rat Model

Somdas¹,

Korkmaz²,

Gürgen³

et al. 2015

Int Adv Otol

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OBJECTIVE:The possible preventive effect of N-acetylcysteine (NAC) in gentamicin ototoxicity was studied with auditory brain stem responses (ABRs), otoacoustic emissions (OAEs), and histopathological investigation of the cochlea. MATERIALS and METHODS:This study is conducted on 36 rats in three groups. Gentamicin, gentamicin plus NAC, and NAC alone were intraperitoneally administered for 15 days. The rats were sacrificed to study the cochleas after testing hearing levels. RESULTS:ABR thresholds and OAEs were attenuated in the gentamicin group, in which apoptosis was detected with histopathological investigation. The group that received NAC in addition to gentamicin had better ABR thresholds and better OAEs. The histopathological evidence of apoptosis in was considerably less in this group. CONCLUSION:Gentamicin ototoxicity can be detected by ABR and OAE testing in rats, and NAC may protect the cochlear cells from apoptosis.

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The role of deferoxamine in the prevention of gentamicin ototoxicity: a histological and audiological study in guinea pigs

Cited by 25 publications

References 12 publications

A Prospective Experimental Study on the Protective Effect of Resveratrol against Amikacin-Induced Ototoxicity in Rats

A Prospective Experimental Study on the Protective Effect of Resveratrol against Amikacin-Induced Ototoxicity in Rats

An aminoglycoside antibiotic gentamycin induces oxidative stress, reduces antioxidant reserve and impairs spermatogenesis in rats

N-acetylcysteine Prevents Gentamicin Ototoxicity in a Rat Model

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