Effects of enrofloxacin and magnesium deficiency on matrix metabolism in equine articular cartilage

Davenport, Celia; Boston, Raymond C.; Richardson, Dean W.

doi:10.2460/ajvr.2001.62.160

Cited by 43 publications

(33 citation statements)

References 32 publications

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“…Chondrotoxic effects of quinolones appear in vitro to be the result of irregular integrin signaling and subsequent cellular changes (Egerbacher et al 2001). Enrofloxacin may have a detrimental effect on cartilage metabolism in horses, especially in neonates (Davenport et al 2001). Degeneration was induced by protease alteration of tendon cells and chondrocytes.…”

Section: Discussionmentioning

confidence: 98%

The effects of enrofloxacin on canine tendon cells and chondrocytes proliferation in vitro

et al. 2007

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Enrofloxacin, a fluoroquinolone antibiotic has been used widely in humans and domestic animals, including dogs, because of its broad-spectrum activity and relative safety. The side effects of fluoroquinolone, induced tendinopathy, tendonitis, spontaneous tendon rupture and cartilage damage, remain incompletely understood. In the present study, we investigated the in vitro effects of enrofloxacin on cell proliferation and induction of apoptosis in canine Achilles tendon cells and chondrocytes. Cell growth and proliferation after treating with enrofloxacin for 2-6 days was quantified by a colorimetric 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxyanilide inner salt (XTT) assay. The results showed that enrofloxacin could inhibit the proliferation of canine tendon cells and chondrocytes at increasing concentrations (10-200 microg/ml). The inhibition of proliferation of canine tendon cells and chondrocytes after exposure to enrofloxacin were associated with induction of apoptosis, as evidenced by the typical nuclear apoptotic condensed nuclei found using Hoechst 33258 staining. It was demonstrated that canine tendon cells and chondrocytes treated with 200 microg/ml enrofloxacin for 4 days exhibited apoptotic features and fragmentation of DNA. Enrofloxacin also increased the apoptosis of canine tendon cells and chondrocytes in a dose and time-dependent manner. The results indicate that enrofloxacin inhibits cell proliferation, induces apoptosis and DNA fragmentation, which might explain enrofloxacin-induced tendinopathy and cartilage damage.

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Section: Discussionmentioning

confidence: 98%

The effects of enrofloxacin on canine tendon cells and chondrocytes proliferation in vitro

et al. 2007

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“…36,37 Susceptibility to cephalosporins varied between gram-negative and gram-positive bacteria. Selection of an antimicrobial for the treatment of foals with septic arthritis should take into account the antimicrobial susceptibility profile of the causative pathogen as well as the potential adverse effects of the drug.…”

Section: Discussionmentioning

confidence: 99%

“…Median (range) values for various variables of the foals ofTable 1that did (n = 47) and did not(36) survive to hospital discharge.…”

mentioning

confidence: 99%

Bacterial isolates, antimicrobial susceptibility patterns, and factors associated with infection and outcome in foals with septic arthritis: 83 cases (1998–2013)

Hepworth-Warren¹,

Wong²,

Fulkerson³

et al. 2015

javma

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“…In vitro toxicity has been demonstrated in tenocytes and chondrocytes (11,84,101), and the chondrotoxicity has been associated with reactive oxygen species (51). Osteoblasts are also sensitive to fluoroquinolones, since these cells produce excess lactate in the presence of therapeutically relevant concentrations of the drug (13).…”

Section: Fluoroquinolones and Chondrotoxicitymentioning

confidence: 99%

Adverse Effects of Antimicrobials via Predictable or Idiosyncratic Inhibition of Host Mitochondrial Components

Barnhill

Brewer

Carlson

2012

Antimicrob Agents Chemother

107

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This minireview explores mitochondria as a site for antibiotic-host interactions that lead to pathophysiologic responses manifested as nonantibacterial side effects. Mitochondrion-based side effects are possibly related to the notion that these organelles are archaic bacterial ancestors or commandeered remnants that have co-evolved in eukaryotic cells; thus, this minireview focuses on mitochondrial damage that may be analogous to the antibacterial effects of the drugs. Special attention is devoted to aminoglycosides, chloramphenicol, and fluoroquinolones and their respective single side effects related to mitochondrial disturbances. Linezolid/oxazolidinone multisystemic toxicity is also discussed. Aminoglycosides and oxazolidinones are inhibitors of bacterial ribosomes, and some of their side effects appear to be based on direct inhibition of mitochondrial ribosomes. Chloramphenicol and fluoroquinolones target bacterial ribosomes and gyrases/topoisomerases, respectively, both of which are present in mitochondria. However, the side effects of chloramphenicol and the fluoroquinolones appear to be based on idiosyncratic damage to host mitochondria. Nonetheless, it appears that mitochondrion-associated side effects are a potential aspect of antibiotics whose targets are shared by prokaryotes and mitochondria-an important consideration for future drug design. SIDE EFFECTS OF ANTIBACTERIAL DRUGST he desired activity of an antibiotic is to kill or prevent the growth of offending pathogenic bacteria, and yet these drugs may impact the host in an injurious manner. Generalized adverse events are common to most antibiotics (e.g., gastrointestinal distress with any oral antibacterial drug), but certain antibiotics are associated with specific effects (Table 1). Some adverse events are mild, e.g., yellowing of the teeth for tetracyclines (77, 79), increased intestinal peristalsis related to erythromycin therapy (7, 67), and reversible orange discoloration of skin and body fluids as observed with rifampin treatment (23, 31). Altered drug metabolism (106) is a common side effect that, in the absence of co-drug therapy, could also be considered mild. More serious side effects include photosensitivity (44) and anaphylactoid reactions (34) observed with many agents, ototoxicity (27, 83) following aminoglycoside therapy, chondrotoxicity (85, 88) and retinopathy (95) with fluoroquinolones, neuropathies associated with metronidazole (30, 107) and linezolid (15), and lactic acidosis and serotonin syndrome attributed to linezolid (21, 61). Other consequences can be severe or even devastating such as: the dermonecrolytic Stevens-Johnson syndrome associated with sulfonamide antimicrobial agents (74, 81); nephrotoxicity related to aminoglycosides (63, 73); aplastic anemia due to chloramphenicol (9, 91); hepatitis caused by many drugs, including isoniazid (72, 89); neuromuscular blockade related to aminoglycoside (64, 65) or lincosamide (4, 70) therapy; myopathies due to ionophores (5, 28, 75); and neoplasia related to metronidazole (19)....

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Effects of enrofloxacin and magnesium deficiency on matrix metabolism in equine articular cartilage

Abstract: Enrofloxacin may have a detrimental effect on cartilage metabolism in horses, especially in neonates.

Cited by 43 publications

References 32 publications

The effects of enrofloxacin on canine tendon cells and chondrocytes proliferation in vitro

The effects of enrofloxacin on canine tendon cells and chondrocytes proliferation in vitro

Bacterial isolates, antimicrobial susceptibility patterns, and factors associated with infection and outcome in foals with septic arthritis: 83 cases (1998–2013)

Adverse Effects of Antimicrobials via Predictable or Idiosyncratic Inhibition of Host Mitochondrial Components

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