There is, I think, something ethereal about i —the square root of minus one. I remember first hearing about it at school. It seemed an odd beast at that time—an intruder hovering on the edge of reality.

Usually familiarity dulls this sense of the bizarre, but in the case of i it was the reverse: over the years the sense of its surreal nature intensified. It seemed that it was impossible to write mathematics that described the real world in …

I and i

Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction

CA : A Cancer Journal for Clinicians

http://europepmc.org/articles/PMC4146684?pdf=render

Cisplatin in cancer therapy: molecular mechanisms of action

Increasing evidence in both experimental and clinical studies suggests that oxidative stress plays a major role in the pathogenesis of both types of diabetes mellitus. Free radicals are formed disproportionately in diabetes by glucose oxidation, nonenzymatic glycation of proteins, and the subsequent oxidative degradation of glycated proteins. Abnormally high levels of free radicals and the simultaneous decline of antioxidant defense mechanisms can lead to damage of cellular organelles and enzymes, increased lipid peroxidation, and development of insulin resistance. These consequences of oxidative stress can promote the development of complications of diabetes mellitus. Changes in oxidative stress biomarkers, including superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase, glutathione levels, vitamins, lipid peroxidation, nitrite concentration, nonenzymatic glycosylated proteins, and hyperglycemia in diabetes, and their consequences, are discussed in this review. In vivo studies of the effects of various conventional and alternative drugs on these biomarkers are surveyed. There is a need to continue to explore the relationship between free radicals, diabetes, and its complications, and to elucidate the mechanisms by which increased oxidative stress accelerates the development of diabetic complications, in an effort to expand treatment options.

Diabetes, oxidative stress, and antioxidants: a review

Thymoquinone (TQ) is the major active component of the volatile oil of Nigella sativa seeds The effects of TQ on carbon tetrachloride (CCl4)-induced hepatotoxicity was investigated in male Swiss albino mice Carbon tetrachloride (20 microliters/Kg, ip) injected into mice, induced damage to liver cells and was followed by the increase in serum alanine aminotransferase (ALT) activity after 24 h Oral administration of TQ in a single dose (100 mg/Kg) resulted in significant (p < 0001) protection against the hepatotoxic effects of CCl4 TQ was tested as a substrate for mice hepatic DT-diaphorase in the presence of NADH TQ appears to undergo reduction to dihydrothymoquinone (DHTQ) Reduction rates as a function of protein (liver homogenate) and substrate (TQ) concentrations are reported An apparent K(m) of 01 mM and an apparent Vmax of 74 mumol/min/g liver were measured TQ and DHTQ inhibited the in vitro non-enzymatic lipid peroxidation in liver homogenate (induced by Fe(3+)-ascorbate) in a dose dependent manner In this in vitro model DHTQ was more potent in comparison with TQ and butylated hydroxytoluene (BHT) The IC50 for DHTQ, TQ and BHT were found to be 034, 087 and 058 microM respectively The data suggest that the in vivo protective action of TQ against CCl4-induced hepatotoxicity may be mediated through the combined antioxidant properties of TQ and its metabolite DHTQ

https://iubmb.onlinelibrary.wiley.com/doi/pdf/10.1080/15216549900201153

Thymoquinone protects against carbon tetrachloride hepatotoxicity in mice via an antioxidant mechanism.

We have evaluated vigabatrin (γ-vinyl γ-aminobutyric acid), an irreversible inhibitor of γ-aminobutyric acid (GABA)-transaminase responsible for GABA degradation, for its effects on food consumption, body weight changes, fluid intake, changes in hematological and biochemical parameters in plasma liver and kidney of Swiss albino mice. Mice received vigabatrin 0.26% wlv chronically in drinking water for 7, 14 and 21 days. Changes in all the parameters were recorded aRer 7, 14 and 21 days respectively in different groups. Food consumption was comparable to the control group with minor fluctuations. The body weight declined significantly but only after 3-week treatment with no appreciable change in organ indices or relative organ indices. There were essentially no adverse effects on hematological parameters (RBC, WBC, HGB, neutrophils, eosinophils, monocytes, lymphocytes and basophils) with this treatment. However, there was a decrease in monocyte counts during the first week and an increase in the neutrophil counts during the third week of vigabatrin treatment. In one part plasma biochemical parameters like AST, ALT, CK-MB, creatinine, glucose and urea were also assessed with the same dose regimen. It was observed that only CK-MB and GPT activity levels were altered slightly significantly and are thought to be a result of cross enzyme inhibitions. In this experiment it was observed that lipid peroxide levels measured, as malondialdehyde did not change appreciably in both liver and kidney tissues. However, the levels of glutathione (non-protein sulfhydryl; GSH) declined significantly in comparison to control in liver and kidney. A comparison of level of GSH in liver and kidney shows that this depletion was at early time points in the former. The depletion of GSH suggests the possible involvement of GSH in detoxification process and corroborates its role in protection.

https://www.mdpi.com/2218-0532/70/2/135/pdf

Effect of Prolonged Vigabatrin Treatment on Hematological and Biochemical Parameters in Plasma, Liver and Kidney of Swiss Albino Mice

The effects of thymoquinone (TQ) on cisplatin-induced nephrotoxicity in mice and rats were studied. Oral administration of TQ (50 mg/L in drinking water) for 5 days before and 5 days after single injections of cisplatin (5 mg/kg, i.v., in rats and 7 or 14 mg/kg, i.p., in mice) greatly ameliorated cisplatin-induced nephrotoxicity in both species. In rats, i.v. cisplatin caused 4- and 5-fold elevations in serum urea and creatinine, a 235% increase in urine volume, a 41% increase in kidney weight, 8.5-fold decrease in creatinine clearance, and extensive histological damage 5 days after treatment. In mice, similar alterations in kidney function were observed. TQ-induced amelioration of cisplatin nephrotoxicity was evident by significant reductions in serum urea and creatinine and significant improvement in polyuria, kidney weight, and creatinine clearance. The protective effects of TQ against cisplatin-induced nephrotoxicity in the rat were further confirmed by histopathological examination. To evaluate the possible modification of the antitumor activity of cisplatin by TQ, we studied their interaction in Ehrlich ascites carcinoma (EAC) bearing mice. The results revealed that TQ potentiated the antitumor activity of cisplatin. The current study suggests that TQ may improve the therapeutic index of cisplatin.

Thymoquinone ameliorates the nephrotoxicity induced by cisplatin in rodents and potentiates its antitumor activity.

Effects of the volatile oil constituents of Nigella sativa, namely, thymoquinone (TQ), p-cymene and alpha-pinene, on carbon tetrachloride (CCl4-indued acute liver injury were investigated in mice. A single dose of CCl4 (15 microl/Kg i.p.) induced hepatotoxicity 24 h after administration manifested biochemically as significant elevation of the enzymes activities of serum alanine transaminase (ALT, EC:2.6.1.2), asparate transaminase (AST, EC:2.6.1.1) and lactate dehydrogenase (LDH, EC: 1.1.1.27). The toxicity was further evidenced by a significant decrease of non-protein sulfhydryl(-SH) concentration, and a significant increase of lipid peroxidation measued as malondialdhyde (MDA) in the liver tissues. Administration of different doses of the TQ (4, 8, 12.5, 25 and 50 mg/Kg i.p.) did not alter the chosen biochemical parameters measured, while higher doses of TQ were lethal. The LD50 was 90.3 mg/Kg (77.9-104.7, 95% CL). Pretreatment of mice with different doses of TQ 1 h before CCl4 injection showed that the only dose of TQ that ameliorated hepatotoxicity of CCl4 was 12.5 mg/Kg i.p. as evidenced by the significant reduction of the elevated levels of serum enzymes as well as hepatic MDA content and significant increase of the hepatic nonprotein sulfhydryl(-SH) concentration. Treatment of mice with the other volatile oil constituents, p-cymene or alpha-pinene did not induce any changes in the serum ALT measured. In addition, i.p. administration of these compounds 1 h before CCl4 injection, did not protect mice against CC4-induced hepatotoxicity. The results of the present study indicate that TQ (12.5 mg/Kg, i.p.) may play an important role as antioxidant and may efficiently act as a protective agent against chemically-induced hepatic damage. In contrast, higher doses of TQ were found to induce oxidative stress leading to hepatic injury.

Effects of volatile oil constituents of Nigella sativa on carbon tetrachloride-induced hepatotoxicity in mice: evidence for antioxidant effects of thymoquinone.

Othman A. Al-Shabanah

Papers

Thymoquinone protects against carbon tetrachloride hepatotoxicity in mice via an antioxidant mechanism.

Effect of Prolonged Vigabatrin Treatment on Hematological and Biochemical Parameters in Plasma, Liver and Kidney of Swiss Albino Mice

Thymoquinone ameliorates the nephrotoxicity induced by cisplatin in rodents and potentiates its antitumor activity.

Effects of volatile oil constituents of Nigella sativa on carbon tetrachloride-induced hepatotoxicity in mice: evidence for antioxidant effects of thymoquinone.

Protective effects of oral arabic gum administration on gentamicin-induced nephrotoxicity in rats.