The production and consumption of paracetamol (4-acetaminophen), a common analgesic and antipyretic drug, had been increased substantially in recent years, elevating the risk of environmental exposure. As an emerging pollutant, this may affect different trophic levels irreversibly and persistently. In this current study, multiple bacterial strains were isolated from pharmaceutical industrial effluents based on paracetamol resistance and primarily screened by non-virulence. Strains PrS3 and PrS14 showed maximum bacterial growth using paracetamol as the sole carbon and nitrogen source. On the contrary, the highest %organic carbon removal efficiency was exhibited by PrS10. The isolates were identified as non-identical and related to the Pseudomonas genus by partial 16S rRNA gene sequencing. The spectrometric assay indicated PrS10 with the highest paracetamol degradation potential (96.37% removal in 7 days), whereas the GC-MS study confirmed 92.35% paracetamol degradation efficiency. The influence of different carbohydrates on paracetamol degradation indicated a competition between monosaccharide and paracetamol as an energy source for PrS10 and reduced degradation efficiency. Further, HR-MS analysis indicated both cell surface absorption as well as the internalization of paracetamol by PrS10. This study explored a probable biodegradation and bioremediation technique for paracetamol contaminants which could be integrated with the effluent treatment of paracetamol production. 

Paracetamol biodegradation by Pseudomonas strain PrS10 isolated from pharmaceutical effluents

This study examined the effect of sodium salicylates (SS), alone and in combination with curcumin (CUR), on kidney function and architecture in rats. Five rat groups were given 1 mL physiological saline/rat orally, 1 mL olive oil/rat orally, 50 mg CUR/kg bwt orally, 300 mg SS/kg bwt intraperitoneally, or CUR+SS for 15 days. The hematological indices, serum protein profile, serum electrolytes balance, oxidative stress, and lipid peroxidation of kidney tissues were assessed. The histopathological examination and immune expression of Caspase-3 and nuclear factor kappa (NF-κB) were conducted. The findings showed that SS injection induced nephrotoxic activity, including increased serum urea, creatinine, and uric acid levels. It also caused apparent pathological alterations with increased Caspase-3 and NF-κB immuno-expression. In addition, thrombocytopenia, leukocytosis, neutrophilia, hyponatremia, hypochloremia, hypocalcemia, and hypomagnesemia but not hyperkalemia and hyperphosphatemia were evident in SS-injected rats. Moreover, SS exposure increased serum α1 globulin, renal tissue malondialdehyde, and Caspase-3 levels but superoxide dismutase, glutathione peroxidase, and Bcl-2 levels declined. Meanwhile, CUR significantly counteracted the SS harmful impacts on kidneys but SS+CUR co-administration induced an anemic condition. Overall, CUR has an evident protective role against SS-induced renal damage, but the disturbed hematological alterations should be carefully taken into consideration in their combined use.

https://www.mdpi.com/2076-3921/10/6/826/pdf

Protective Effect of Curcumin against Sodium Salicylate-Induced Oxidative Kidney Damage, Nuclear Factor-Kappa Dysregulation, and Apoptotic Consequences in Rats.

Paracetamol (PAR) is a commonly used antipyretic and analgesic agent, but its excessive usage can induce liver damage and major health consequences. Interleukin-35 (IL-35) is utilized to treat immunological disorders, intestinal illness, arthritis, allergic disease, hepatitis, and cancer. Thymoquinone (THYO) is also effective against a wide range of disorders. Consequently, this study sought out to explore the ameliorative effects of IL-35 and THYO against PAR-induced hepatotoxicity in rats. Sixty male rats were separated into six groups (10 rats/group): I control (0.5 mL NaCl, 0.9%/rat via oral gavage); II (IL-35), and III (TYHO) received intraperitoneal (i.p) injection of IL-35 (200 ng/kg) or THYO (0.5 mg/kg), respectively. Group IV (PAR) received 600 mg/kg of PAR orally; V (PAR+IL-35) and VI (PAR+TYHO); rats received 600 mg/kg of PAR orally and i.p injection of IL-35 (200 ng/kg) or THYO (0.5 mg/kg), respectively. Administration of IL-35 or THYO markedly mitigated the increasing in the levels of liver parameters triggered by PAR and noticeable enhancement of antioxidant and immunological markers were observed. Additionally, IL-35 or THYO decreased TNF-α, NF-κB, IL-10, IL-6 and IFN-γ in contrast to the PAR control group. Moreover, levels of Capase-3, and cytochrome C were significantly reduced by THYO or IL35, while, levels of Bcl-2 were markedly increased. Furthermore, significant downregulation of IL1-β, TNF-α, TGF-β, and Caspas-3 genes, as well as significant upregulation of Bcl-2 and IL-10 expression were detected. In conclusion, IL-35 and THYO insulated liver from PAR toxicity by mitigating oxidative stress, tissue damage, inflammation, and apoptosis. 

Interleukin-35 and Thymoquinone nanoparticle-based intervention for liver protection against paracetamol-induced liver injury in rats

Paracetamol is a popular analgesic drug and its overdose may cause toxicity in the kidney. Prunus laurocerasus L. (PL) is an important folklore medicinal plant that has antioxidant properties. This study explores effects of PL fruit water and ethanol-water extracts administrations on oxidative stress in paracetamol-induced nephrotoxicity. For this purpose, 30 rats were divided into 5 groups: control, negative control (2 g/kg paracetamol), PL fruit water extract (400 mg/kg PLW+ 2 g/kg paracetamol), PL fruit ethanol-water extract (400 mg/kg PLEW+ 2 g/kg paracetamol) and positive control (150 mg/kg NAC+ 2 g/kg paracetamol). 24 hours after the paracetamol induction, animals were sacrificed and oxidative parameters were analyzed spectrophotometrically in kidney tissue. PLW and PLEW extracts decreased MDA and NOx levels and increased SOD and CAT activities in paracetamol-induced nephrotoxicity. PL fruit extracts can restore the oxidative changes caused by paracetamol.

Prunus laurocerasus L. extracts prevent paracetamol-induced nephrotoxicity by regulating antioxidant status: an experimental animal model

This study aims to investigate the effects of Ozone therapy used in traditional and complementary medicine on possible toxicity caused by Acetaminophen (APAP). There was no intervention in first group (control). The second group received 150 µg·kg-1 day, i.p. for three weeks of ozone, 2 g·kg-1 orally single dose APAP to third group, and APAP+Ozone to fourth group. APAP was administered on 21st day of ozone application. Malondialdehyde (MDA) levels, reduced glutathione (GSH) levels, and antioxidant enzyme activities were all measured to assess their contribution to pathogenesis of toxicity in blood tissues. Compared to the control group, the group receiving APAP showed increased MDA levels (P=0.009) and decreased GSH levels (P<0.001), as well as reduced CAT (P<0.001), GSH–Px (P<0.001) and SOD (P<0.001) enzyme activities. However, in the group treated with ozone and APAP, levels of MDA and GSH, as well as the activities of the antioxidant enzymes, were similar to those of the control group, indicating a protective effect of ozone against APAP–induced oxidative stress. In conclusion, the results of the study showed that APAP caused oxidative stress in blood tissue. The present study showed that ozone had potential protective effects against toxicity induced with APAP through various mechanisms in different cellular processes. This may be related to cytoprotective and antioxidant properties of ozone. Ozone can provide a chemical basis for some health benefits against toxicities. Ozone may be protective against APAP–induced oxidative damage. As a result, it was concluded that ozone may be a natural and effective antioxidant that can be used to reduce the toxicity caused by APAP.

Evaluation of the effects of overdose Acetaminophen toxicity in rats: Ozone, which can be preferred as a complementary therapy

Since paracetamol was produced by pharmaceutical companies in 1960, many cases of hepatotoxicity and nephrotoxicity were reported due to the use of paracetamol overdoses. Some small paracetamol is metabolized to toxic N-acetyl-p-benzoquinone imine (NAPQI) by cytochrome P450, especially CYP2E1. NAPQI plays a major role in the mechanism of hepatotoxicity and nephrotoxicity. Curcuma longa as an antioxidant and anti-inflammatory can prevent damage to hepatic and renal cells.

Curcumin, antioxidant activity, and paracetamol toxicity

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Curcumin, antioxidant activity, and paracetamol toxicity