Table 1.

The pathological changes associated with metals/NPs-mediated autophagy regulation

Metals/NPs	Autophagic activity	Toxicity of Metal/NPs	Pathological changes	References
Cd	Inhibition	Increase	Hepatic steatosis Glomerular atrophy	[183] [184]
	Activition	Increase	Renal tubular dilatation Hepatic lobular injury Renal cortex injury	[185] [186] [187]
Cr	Activition	Increase	Renal tubular rupture Damage of liver mitochondria Cardiomyocyte necrosis Blurred boundaries of glomerula	[80] [188] [189] [190]
Pb	Inhibition	Increase	Structural changes of the spleen, ferritin deposits	[191]
	Activition	Increase	Hippocampus damage	[192]
As	Inhibition	Increase	Skin tumorigenesis	[193]
	Activition	Increase	Islet cell hypertrophy Glomerular atrophy Aortic injuries Mitochondrial damage in jejunal cells Testicular tissue damage Purkinje cell layer damage Hepatic steatosis Liver fibrosis	[194] [195] [196] [197] [198] [199] [200] [201]
Hg	Inhibition	Increase	Tubular necrosis, interstitial hyperemia, and inflammatory cell infiltration	[202]
	Activition	Increase	Spleen damage	[203]
Al	Activition	Increase	Femoral damage	[204]
	Activition	Decrease	Testicular damage Liver inflammatory injury	[205] [206]
NPs	Activition	Increase	Neurovascular toxicity	[207]
	Activition	Decrease	Liver damage	[208]

Activation/Inhibition represents that the autophagy is activated or inhibited by the metals/NPs. Increase/Decrease represents that the autophagic activity enhances or attenuates the toxicity of the metals/NPs.