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Background <p>Diabetic cataract remains a prominent complication of diabetes mellitus, predominantly driven by oxidative stress and low-grade inflammation in the lens. Despite surgical remedies, efficacious pharmacological interventions to delay or prevent cataract progression are limited. L-tartaric acid, a naturally occurring dicarboxylic organic acid, exhibits notable antioxidative and anti-inflammatory properties, suggesting its potential therapeutic value in diabetic lens pathology.</p> Methods <p>This study explored the effects of L-tartaric acid on cataractogenesis in a streptozotocin (STZ)-induced diabetic rat model. Oral administration of L-tartaric acid (50 mg/kg/day) or vehicle commenced one-week post-diabetes induction and continued for 12 weeks. Cataract formation was evaluated via biomicroscopic scoring. Biochemical analyses of oxidative stress markers (malondialdehyde and antioxidant enzymes) and inflammation-related cytokines were conducted, alongside quantitative PCR to assess the expression of inflammation-related cytokines and transcription factors Nrf2 and NF-κB in lens tissues.</p> Results <p>Chronic hyperglycemia significantly elevated oxidative damage and pro-inflammatory mediators in the lens, culminating in advanced cataract formation in untreated diabetic rats. In contrast, L‑tartaric acid treatment markedly reduced the incidence and severity of cataracts, lowering the proportion of lenses with advanced opacities (score ≥ 3) from 80 to 30%, a 62.5% relative reduction, concomitantly attenuating lipid peroxidation and improving antioxidant enzyme activities. Notably, L-tartaric acid suppressed pro-inflammatory cytokine expression and restored Nrf2 and NF-κB to near-normal levels, without altering blood glucose concentrations.</p> Conclusion <p>L‑tartaric acid significantly reduces oxidative damage and inflammation in the lens, and shows potential in protecting against diabetic cataract by reinforcing the endogenous antioxidant defense network and moderating inflammatory processes. These data suggest that L‑tartaric acid may serve as a promising adjunct therapy to curb the onset and progression of diabetic cataract, possibly through mechanisms independent of glycemic control. Further studies, including topical formulations and well-designed human clinical trials, are needed to validate these preliminary observations.</p>

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The effects of L-tartaric acid on diabetic cataracts through modulation of oxidative stress and inflammation in diabetic rats

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月3日

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  • Shengyu Wang,
  • Li Meng,
  • Hengmin Yang

摘要

Background

Diabetic cataract remains a prominent complication of diabetes mellitus, predominantly driven by oxidative stress and low-grade inflammation in the lens. Despite surgical remedies, efficacious pharmacological interventions to delay or prevent cataract progression are limited. L-tartaric acid, a naturally occurring dicarboxylic organic acid, exhibits notable antioxidative and anti-inflammatory properties, suggesting its potential therapeutic value in diabetic lens pathology.

Methods

This study explored the effects of L-tartaric acid on cataractogenesis in a streptozotocin (STZ)-induced diabetic rat model. Oral administration of L-tartaric acid (50 mg/kg/day) or vehicle commenced one-week post-diabetes induction and continued for 12 weeks. Cataract formation was evaluated via biomicroscopic scoring. Biochemical analyses of oxidative stress markers (malondialdehyde and antioxidant enzymes) and inflammation-related cytokines were conducted, alongside quantitative PCR to assess the expression of inflammation-related cytokines and transcription factors Nrf2 and NF-κB in lens tissues.

Results

Chronic hyperglycemia significantly elevated oxidative damage and pro-inflammatory mediators in the lens, culminating in advanced cataract formation in untreated diabetic rats. In contrast, L‑tartaric acid treatment markedly reduced the incidence and severity of cataracts, lowering the proportion of lenses with advanced opacities (score ≥ 3) from 80 to 30%, a 62.5% relative reduction, concomitantly attenuating lipid peroxidation and improving antioxidant enzyme activities. Notably, L-tartaric acid suppressed pro-inflammatory cytokine expression and restored Nrf2 and NF-κB to near-normal levels, without altering blood glucose concentrations.

Conclusion

L‑tartaric acid significantly reduces oxidative damage and inflammation in the lens, and shows potential in protecting against diabetic cataract by reinforcing the endogenous antioxidant defense network and moderating inflammatory processes. These data suggest that L‑tartaric acid may serve as a promising adjunct therapy to curb the onset and progression of diabetic cataract, possibly through mechanisms independent of glycemic control. Further studies, including topical formulations and well-designed human clinical trials, are needed to validate these preliminary observations.