Endotoxin increases the nephrotoxic potential of gentamicin and vancomycin plus gentamicin

Article Abstract:

Endotoxin is found in the cell walls of gram-negative bacteria (a class of bacteria that do not stain with Gram stain). In humans with gram-negative bacterial infections, endotoxin stimulates the production of proteins that can cause inflammation, low blood pressure and kidney damage. Patients with serious life-threatening illnesses, which may include gram-negative bacterial infections, are being treated more often with aminoglycoside drugs. These drugs are known for their ability to cause kidney damage (nephrotoxicity). Studies in humans have shown that the antibiotic vancomycin, by itself, does not cause kidney damage. However, when vancomycin was given together with an aminoglycoside drug, kidney damage was apparent in 35 percent of the patients receiving the treatment. The combined effects of aminoglycoside therapy and endotoxin on nephrotoxicity have not been determined. To address this issue, rats were given intravenous endotoxin or saline along with vancomycin, gentamicin, or both. Following five to eight days of treatment kidney function tests were performed and histological samples were evaluated. Of the treated rats, only those receiving the combination of gentamicin and vancomycin showed abnormalities. Endotoxin did not cause kidney damage in rats treated with vancomycin alone. Rats treated with endotoxin and gentamicin, or with endotoxin plus gentamicin plus vancomycin, developed signs of kidney damage. It is concluded that endotoxin enhances the nephrotoxicity of gentamicin alone and gentamicin plus vancomycin. (Consumer Summary produced by Reliance Medical Information, Inc.)

Injuries, Complications and side effects, Vancomycin, Kidneys, Endotoxins, Kidney, Aminoglycosides, Gentamicin, Gentamicins

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Uptake and binding of liposomal 2',3'-dideoxycytidine by RAW 264.7 cells: a three-step process

Article Abstract:

Fat complexes called liposomes may facilitate the accumulation and retention of an HIV inhibitor in immune system cells. Researchers found that accumulation and retention of the anti-HIV drug dideoxycytidine in immune system cells known as macrophages was enhanced by incorporating the drug into liposomes. Macrophages disseminate HIV to other cell types and are believed to be very involved in the development of AIDS. Blood proteins may facilitate the ingestion of liposomes by macrophages. In addition to blood proteins, the size and positive or negative charge of liposomes may determine drug delivery. Liposomes may help HIV inhibitors bind to transporters of sugars known as nucleosides. This finding may allow drug developers to use liposomes to create better drug delivery systems for anti-HIV drugs.

Research, Usage, Macrophages, Liposomes, Zalcitabine

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Antiviral efficacy and toxicity of ribavirin in murine acquired immunodeficiency syndrome model

Article Abstract:

Ribavirin can protect animals against murine acquired immunodeficiency syndrome (MAIDS) but can be toxic to red blood cells in high dosage. An aerosol antiviral drug, Ribavirin resembles the nucleotide guanosine and can be effective against DNA and RNA viruses. The disease in mice, MAIDS shows similarities to HIV in humans except that MAIDS targets B-cells rather than T-cells. If given to mice in 50 milligram per kilogram doses ribavirin can prevent MAIDS and protect the spleen and lymph nodes from infection. Ribavirin caused anemia and toxicity in mice at 50 mg/kg to 100 mg/kg doses.

Evaluation, HIV infection, HIV infections, Antiviral agents, Ribavirin, Mouse leukemia viruses

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