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NG orally to mice 30 min before oral administration of cadmium chloride (12 mg/kg) for 11

days and observed that NG significantly normalised hematological profiles, and serum
biochemical profiles and modulated the liver and kidney biochemical parameters in Cd-

intoxicated mice.
Fouad et al. (2020) demonstrated the protective effects of NG in the pancreatic injury

and dysfunction caused by cadmium chloride in rats. Cd administration caused significant
increase of MDA, tumor necrosis factor-α, interleukin-1β, nuclear factor-κB p65, Bax/Bcl-2

ratio, phosphorylated c-Jun N-terminal kinase (p-JNK) and p38 MAPKs and significant

decrease of GSH and CAT in the pancreas of rats. While as NG ameliorated the toxic effects
of Cd in pancreas via modulating the JNK and p38 MAPKs signaling pathways and inhibition

of oxidative stress.

The effect of NG on Cd induced testicular toxicity was studied in male Sprague–
Dawley rats by Wang et al. (2021). Rats were administered with CdCl2 (2 mg/kg b.w.

intraperitoneally), NG (50 mg/kg b.w, orally), and CdCl2 + NG (2 mg/kg b.w
intraperitoneally and 50 mg/kg b.w. orally, respectively) for 4 weeks. They observed decrease

in body weight, relative testes weights, and sperm quality in the Cd-treated group, as well as
Cd accumulated in serum and testes. Cd reduced the serum concentrations of GnRH, FSH,

LH, and testosterone. Also, the decreased activities of SOD, CAT, GPx, GSH content and

increased MDA and H2O2 contents were observed in Cd treated groups. They found that Cd
activated autophagy in testis by upregulating the expression of the autophagy-related proteins

P62 and LC3 II. However, administration of NG significantly attenuated the Cd-induced
negative effects by increasing the body weight, relative testis weights, and sperm quality and

by decreasing testicular damage. NG administration simultaneously restored the decreased
levels of GnRH, FSH, LH, testosterone, GSH, and the activities of SOD, CAT, and GPx.

Further, NG decreased MDA and H2O2 production and protected the testes from Cd-induced

autophagy by downregulating P62 and LC3 II expression. Thus, they suggested that Cd
induced testicular toxicity can be improved with NG by increasing the total antioxidant

capacity, improving histology and reducing germ-cell autophagy.

6. CONCLUSION

In this review, we have summarised the recent studies demonstrating the properties of

NG and its role in providing protection from Cd intoxication in animal models. NG has been
found to be a promising compound to exert protective effects against Cd induced toxicity.

These beneficial effects of NG are attributed to antioxidant and free radical scavenging

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