No abstract

Highlights PM produced oxidative stress in gastric, liver, and kidney tissue. PM-induced toxicity was mediated by ROS and mitochondrial dysfunction. PM enhanced the activated caspase-3 expression. CoQ10 alleviates PM-induced gastropathy and hepato-renal damage. CoQ10 might be effective in COVID-19 treatment regimen.

Although the combination of antibiotics is generally well-tolerated, they may have nephrotoxic effects. This study investigated whether tigecycline (TG) and gentamicin (GM) co-administration could accelerate renal damage. Male Wistar rats were randomly divided into six experimental groups: the control, TG7 (tigecycline, 7 mg/kg), TG14 (tigecycline, 14 mg/kg), GM (gentamicin, 80 mg/kg), TG7+GM, and TG14+GM groups. The combination of TG and GM evoked renal damage seen by the disruption of kidney function tests. The perturbation of renal tissue was mainly confounded to the TG and GM-induced oxidative damage, which was exhibited by marked increases in renal MDA (malondialdehyde) along with a drastic reduction in GSH (reduced-glutathione) content and CAT (catalase) activity compared to their individual treatments. More obvious apoptotic events and inflammation were also revealed by elevating the annexin-V and interleukin-6 (IL-6) levels, aside from the upregulation of renal PCNA (proliferating cell nuclear antigen) expression in the TG and GM concurrent treatment. The principal component analysis indicated that creatinine, urea, annexin-V, IL-6, and MDA all played a role in discriminating the TG and GM combined toxicity. Oxidative stress, inflammatory response, and apoptosis were the key mechanisms involved in this potentiated toxicity.

Tigecycline (TIG) toxicity is a threat to health because of the mortality risk attributed to its overdose. Large doses result in fatal cardiomyopathy and acute cardiotoxicity. Gentamicin (GEN) is an aminoglycoside antibacterial agent that affects kidney function, causing nephrotoxicity. Six groups of rats (n=5) were used. Control (DW), TIG 7 (TIG 7 mg/kg IP), TIG14 (TIG 14 mg/kg IP), gentamicin (GEN), TIG 7+ GEN, and TIG 14+ GEN groups. Cardiac catalase (CAT) activity, glutathione (GSH), and malondialdehyde (MDA) levels in the heart, as well as histopathological changes were recorded. Myocardium from TIG 14+ GEN group exhibited typical changes for myocardial apoptosis and degeneration, as well as an increase in interleukin-6 (IL-6) and annexin-V levels, were recorded specially in the TIG 14+ GEN group. GEN, in addition to its nephrotoxicity, increases TIG-induced cardiotoxicity. GEN may increase the cardiotoxicity of high dose TIG. Particularly large doses of GEN have a negative impact on the cardiac oxidative stress caused by TIG.

In most diseases, concurrent exposure to antibacterial is essential. The purpose of this research is to determine how co-administration of the antibiotics gentamicin (an aminoglycoside) and tigecycline (a tetracycline) affects the liver of rats. Rats received distilled water, tigecycline 7 (TIG 7), tigecycline 14 (TIG14), gentamicin (GEN), tigecycline 7 + gentamicin, and tigecycline 14 + gentamicin groups. After 10 days, TIG and/or GEN caused tissue damage that is seen in considerable biochemical changes in assays of liver functions. Also, a significant elevation of AST, ALT, ALP, cholesterol, and a significant decrease in albumin after TIG or GEN treatment when compared to control groups were observed. A considerable increase in these parameters was observed following TIG and GEN combination. Besides this, there were noticeable pathological alterations in the tissues of the liver. In addition, after TIG and GEN treatment, there is a considerable overexpression of PCNA in the tissues of the liver. As a result, TIG and GEN therapy administered together caused more evident liver damage than either therapy administered individually. According to the findings overall, using TIG and GEN simultaneously in clinical practice is concerning, so it should be done with caution to prevent synergistic negative results.