Quercetin Dihydrate And Oxidative Stress: Mouse Study Summary

The study “Exploring the Potential Role of Quercetin Dihydrate Against Carbon Tetrachloride Induced Oxidative Stress in Mice: A Randomized Controlled Trial” (Asghar et al., 2025) used a CCl4 mouse model to examine how quercetin dihydrate relates to oxidative stress markers in multiple tissues. Male mice were assigned to four groups, including a negative control, a CCl4-only group, and two quercetin dihydrate groups (60 or 120 mg/kg body weight) given before a CCl4 challenge. Outcomes included MDA and CAT measured in the liver, muscle, and kidney. The paper reports that CCl4 shifted these markers versus the negative control and that the quercetin dihydrate groups differed from the CCl4-only group for several reported outcomes. This overview restates the study for educational purposes and is not treatment guidance.

The paper describes oxidative stress as an imbalance between reactive oxygen species (ROS) and antioxidant defenses, which can disrupt redox balance and contribute to lipid, protein, and DNA damage. The focus in this study is on a toxin-triggered mouse model, not a test of disease outcomes or clinical benefits.

The paper describes CCl4 as a common laboratory chemical used in animal research to trigger oxidative stress and tissue injury through reactive metabolites. It is metabolized by cytochrome P450 to reactive trichloromethyl and peroxy-trichloromethyl radicals, which attack lipids, proteins, and DNA and trigger lipid peroxidation. CCl4 metabolism also activates liver Kupffer cells and promotes pro-inflammatory cytokine release, which further increases oxidative stress and suppresses antioxidant enzymes. The paper describes CCl4 exposure as a driver of lipid peroxidation and reports MDA as one marker used to reflect that process in animal research.

Quercetin is a natural flavonoid polyphenol found in many fruits and vegetables. Quercetin dihydrate is a commercially available crystalline form that is more thermodynamically stable under normal conditions than some other quercetin forms and is sold as a bright yellow powder. Previous experimental work has shown that quercetin can scavenge ROS and reduce oxidative damage in different models, including acrylamide toxicity, radiation-induced brain injury, heavy metal-related nerve damage, and nanoparticle-induced nephrotoxicity. Based on this background, the study examined whether quercetin dihydrate was associated with changes in oxidative stress markers in the liver, muscle, and kidney after a CCl4 challenge.

The paper describes 24 healthy male mice randomly allocated to four experimental groups in a randomized controlled design. The key groups were:

• QC (control negative): standard chow and water, with a single intraperitoneal (IP) dose of normal saline on day 21.
• Q0 (control positive): standard diet plus oral saline for 20 days, then a single IP injection of CCl4 prepared in a carrier oil at 1 mL/kg body weight on day 21.
• Q1 (quercetin dihydrate 60 mg/kg): daily oral quercetin dihydrate at 60 mg/kg body weight for 20 days, followed by the same CCl4+olive oil injection on day 21.
• Q2 (quercetin dihydrate 120 mg/kg): daily oral quercetin dihydrate at 120 mg/kg body weight for 20 days, followed by CCl4+olive oil on day 21.

Animals were kept under controlled temperature, given time to acclimatize, and monitored daily for general condition. At the end of the experimental period, mice were fasted for about 12 hours, anesthetized, and then blood, liver, kidney, and muscle tissues were collected. Tissues were weighed, homogenized in cold phosphate-buffered saline, and centrifuged. The supernatant was used to measure oxidative stress markers.

MDA, a marker of lipid peroxidation, was quantified using a thiobarbituric acid (TBA) reaction, where MDA reacts with TBA to form a red complex measured spectrophotometrically at 535 nm. CAT activity was assessed by measuring undecomposed hydrogen peroxide (H2O2) reacting with ammonium molybdate to give a yellow color read at 374 nm. Data were expressed as mean ± standard error, analyzed with one-way ANOVA and post hoc tests, with p < 0.05 considered statistically significant.

CCl4 exposure (Q0) was reported to increase MDA in the liver, muscle, and kidney compared with the negative control. Quercetin dihydrate groups (Q1 and Q2) were reported to have lower MDA than the CCl4-only group across these tissues, consistent with reduced lipid peroxidation in this model, as described in the paper.

Similar patterns were seen in the muscle and the kidney. Muscle MDA rose in the CCl4-only group but was significantly decreased in both quercetin dihydrate groups. Kidney MDA also increased with CCl4 and fell again in the Q1 and Q2 groups. The authors interpret this as evidence that quercetin dihydrate reduced CCl4-induced lipid peroxidation and helped limit oxidative damage in all three tissues.

In the liver and muscle, CCl4 exposure lowered CAT activity compared with the negative control, showing a weakened antioxidant defense. Quercetin dihydrate supplementation significantly increased liver and muscle CAT activity compared with the CCl4-only group, bringing values close to those of the negative control animals. The authors state that quercetin dihydrate “significantly restored the redox status” by boosting antioxidant enzyme activity.

In the kidney, the pattern was different. While CCl4 reduced CAT activity, the increase with quercetin dihydrate in Q1 and Q2 did not reach statistical significance (p = 0.333), so the paper reports no clear improvement in renal CAT activity, despite the decrease in kidney MDA. This suggests partial protection in the kidney, more evident in lipid peroxidation markers than in that specific antioxidant enzyme.

Both quercetin dihydrate doses, 60 and 120 mg/kg body weight, lowered MDA and improved CAT in the liver and muscle compared with CCl4 alone. In liver, the 120 mg/kg group showed the lowest MDA level, but Q1 and Q2 often shared the same statistical superscript in the table, meaning the differences between the two doses were not always significant. The authors therefore emphasize the general protective effect of quercetin dihydrate at both doses, rather than claiming a consistent, marker-by-marker advantage of 120 mg/kg over 60 mg/kg.

The paper concludes that quercetin dihydrate was associated with lower MDA and higher CAT activity in this CCl4 mouse model, reflecting marker changes consistent with improved antioxidant marker balance in several tissues. The results describe clearer CAT increases in liver and muscle, with kidney findings showing reduced MDA and less clear CAT changes.

The discussion notes that this work is an animal model and calls for additional mechanistic research, including molecular pathway studies, to clarify how these marker changes occur.

All implications in this section are paraphrased from the authors’ discussion and are presented for educational purposes only. This summary does not provide medical advice and does not suggest quercetin dihydrate for disease treatment, cure, or prevention in humans.

In this 2025 mouse study, quercetin dihydrate at 60 or 120 mg/kg body weight given for 20 days before a CCl4 challenge was reported to lower MDA in liver, muscle, and kidney, with CAT activity increases reported most clearly in liver and muscle. These findings describe changes in oxidative stress markers within a toxin-based animal model. This page paraphrases the published paper for educational use and does not provide medical guidance.